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human colorectal cell line hct116  (ATCC)


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    ATCC human colorectal cell line hct116
    Postbiotic Pd modifies mitochondria in a colon cell line. (A) Right panel-representative images of <t>HCT116</t> treated or not with postbiotic Pd for 24h and labeled with TMRE to determine mitochondrial morphology. Bar = 10 µm. Left panel- bar graphs of the mitochondrial length analysis. Data are expressed as MEAN ± SEM of five independent experiments ****p≤0.0001. Mann-Whitney test . (B) Upper panel- representative Western blot of PGC1α and GADPH as a loading control in HCT116 cells treated or not with postbiotic Pd. Bottom panel- Bar graphs represent quantification of PGC1α/GADPH expressed as MEAN ± SEM of five independent experiments. ∗p < 0.05. Mann-Whitney test . (C) Upper panel- representative Seahorse trace of HCT116 cells treated or not with postbiotic Pd. A; oligomycin (1 µM), B;FCCP (250 µM), C; rotenone plus antimycin A (1 µM each). Bottom panel- basal and maximum OCR of HCT116 cells treated or not with postbiotic Pd. MEAN ± SEM of three independent experiments with 10 replicates each. ***P < 0.001 compared to control. Mann-Whitney test. (D) Upper panel- representative Western blot of CHOP and β-actin as a loading control in HCT116 cells treated or not with postbiotic Pd. Bottom panel- bar graphs represent quantification of CHOP/β-actin expressed as MEAN ± SEM of 3 independent experiments. ∗p < 0.05. Mann-Whitney test . (E) Upper panel- representative Western blot of VDAC1 and β-actin as a loading control in colon mucosa samples from 26-months-old mice treated or not with postbiotic Pd. Bottom panel- bar graphs represent quantification of VDAC1/β-actin expressed as MEAN ± SEM. Note that β-actin blot in is the same as in this figure, as the same membrane was stripped and re-probed for VDAC1. N = 3 in the control group and 4 for the Pd treated group. ∗p < 0.05. Mann-Whitney test .
    Human Colorectal Cell Line Hct116, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 4085 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+colorectal+cell+line+hct116/HCT+116/pmc13061540-127-0-5
    Average 99 stars, based on 4085 article reviews
    human colorectal cell line hct116 - by Bioz Stars, 2026-09
    99/100 stars

    Images

    1) Product Images from "Postbiotic Parabacteroides Distasonis Supplementation Enhances Intestinal and Skeletal Muscle Function in Aged Mice"

    Article Title: Postbiotic Parabacteroides Distasonis Supplementation Enhances Intestinal and Skeletal Muscle Function in Aged Mice

    Journal: Aging and Disease

    doi: 10.14336/AD.2025.0188

    Postbiotic Pd modifies mitochondria in a colon cell line. (A) Right panel-representative images of HCT116 treated or not with postbiotic Pd for 24h and labeled with TMRE to determine mitochondrial morphology. Bar = 10 µm. Left panel- bar graphs of the mitochondrial length analysis. Data are expressed as MEAN ± SEM of five independent experiments ****p≤0.0001. Mann-Whitney test . (B) Upper panel- representative Western blot of PGC1α and GADPH as a loading control in HCT116 cells treated or not with postbiotic Pd. Bottom panel- Bar graphs represent quantification of PGC1α/GADPH expressed as MEAN ± SEM of five independent experiments. ∗p < 0.05. Mann-Whitney test . (C) Upper panel- representative Seahorse trace of HCT116 cells treated or not with postbiotic Pd. A; oligomycin (1 µM), B;FCCP (250 µM), C; rotenone plus antimycin A (1 µM each). Bottom panel- basal and maximum OCR of HCT116 cells treated or not with postbiotic Pd. MEAN ± SEM of three independent experiments with 10 replicates each. ***P < 0.001 compared to control. Mann-Whitney test. (D) Upper panel- representative Western blot of CHOP and β-actin as a loading control in HCT116 cells treated or not with postbiotic Pd. Bottom panel- bar graphs represent quantification of CHOP/β-actin expressed as MEAN ± SEM of 3 independent experiments. ∗p < 0.05. Mann-Whitney test . (E) Upper panel- representative Western blot of VDAC1 and β-actin as a loading control in colon mucosa samples from 26-months-old mice treated or not with postbiotic Pd. Bottom panel- bar graphs represent quantification of VDAC1/β-actin expressed as MEAN ± SEM. Note that β-actin blot in is the same as in this figure, as the same membrane was stripped and re-probed for VDAC1. N = 3 in the control group and 4 for the Pd treated group. ∗p < 0.05. Mann-Whitney test .
    Figure Legend Snippet: Postbiotic Pd modifies mitochondria in a colon cell line. (A) Right panel-representative images of HCT116 treated or not with postbiotic Pd for 24h and labeled with TMRE to determine mitochondrial morphology. Bar = 10 µm. Left panel- bar graphs of the mitochondrial length analysis. Data are expressed as MEAN ± SEM of five independent experiments ****p≤0.0001. Mann-Whitney test . (B) Upper panel- representative Western blot of PGC1α and GADPH as a loading control in HCT116 cells treated or not with postbiotic Pd. Bottom panel- Bar graphs represent quantification of PGC1α/GADPH expressed as MEAN ± SEM of five independent experiments. ∗p < 0.05. Mann-Whitney test . (C) Upper panel- representative Seahorse trace of HCT116 cells treated or not with postbiotic Pd. A; oligomycin (1 µM), B;FCCP (250 µM), C; rotenone plus antimycin A (1 µM each). Bottom panel- basal and maximum OCR of HCT116 cells treated or not with postbiotic Pd. MEAN ± SEM of three independent experiments with 10 replicates each. ***P < 0.001 compared to control. Mann-Whitney test. (D) Upper panel- representative Western blot of CHOP and β-actin as a loading control in HCT116 cells treated or not with postbiotic Pd. Bottom panel- bar graphs represent quantification of CHOP/β-actin expressed as MEAN ± SEM of 3 independent experiments. ∗p < 0.05. Mann-Whitney test . (E) Upper panel- representative Western blot of VDAC1 and β-actin as a loading control in colon mucosa samples from 26-months-old mice treated or not with postbiotic Pd. Bottom panel- bar graphs represent quantification of VDAC1/β-actin expressed as MEAN ± SEM. Note that β-actin blot in is the same as in this figure, as the same membrane was stripped and re-probed for VDAC1. N = 3 in the control group and 4 for the Pd treated group. ∗p < 0.05. Mann-Whitney test .

    Techniques Used: Labeling, MANN-WHITNEY, Western Blot, Control, Membrane

    Related Articles

    Labeling:

    Article Title: Postbiotic Parabacteroides Distasonis Supplementation Enhances Intestinal and Skeletal Muscle Function in Aged Mice
    Article Snippet: Human colorectal cell line HCT116 (ATCC) was maintained at 37oC (95%/5% air/CO 2 ) in DMEM media (GIBCO) supplemented with 10% (v/v) FBS.. Skeletal muscle cell line Hskm was maintained at 37oC (95%/5% air/CO 2 ) in αMEM/F12 supplemented with 200mM L-glutamine, 1% FBS, 1mg/ml EGF, 0.1 mg/mL βFGF, 100UI/mL insulin and 10mM dexamethasone.Skeletal muscle cell line Hskm was maintained at 37oC (95%/5% air/CO 2 ) in αMEM/F12 supplemented with 200mM L-glutamine, 1% FBS, 1mg/ml EGF, 0.1 mg/mL βFGF, 100UI/mL insulin and 10mM dexamethasone.

    Article Title: Postbiotic <i>Parabacteroides Distasonis</i> Supplementation Enhances Intestinal and Skeletal Muscle Function in Aged Mice
    Article Snippet: Human colorectal cell line HCT116 (ATCC) was maintained at 37oC (95%/5% air/CO2) in DMEM media (GIBCO) supplemented with 10% (v/v) FBS.. Skeletal muscle cell line Hskm was maintained at 37oC (95%/5% air/CO2) in αMEM/F12 supplemented with 200mM Lglutamine, 1% FBS, 1mg/ml EGF, 0.1 mg/mL βFGF, 100UI/mL insulin and 10mM dexamethasone.Skeletal muscle cell line Hskm was maintained at 37oC (95%/5% air/CO2) in αMEM/F12 supplemented with 200mM Lglutamine, 1% FBS, 1mg/ml EGF, 0.1 mg/mL βFGF, 100UI/mL insulin and 10mM dexamethasone.

    MANN-WHITNEY:

    Article Title: Postbiotic Parabacteroides Distasonis Supplementation Enhances Intestinal and Skeletal Muscle Function in Aged Mice
    Article Snippet: Human colorectal cell line HCT116 (ATCC) was maintained at 37oC (95%/5% air/CO 2 ) in DMEM media (GIBCO) supplemented with 10% (v/v) FBS.. Skeletal muscle cell line Hskm was maintained at 37oC (95%/5% air/CO 2 ) in αMEM/F12 supplemented with 200mM L-glutamine, 1% FBS, 1mg/ml EGF, 0.1 mg/mL βFGF, 100UI/mL insulin and 10mM dexamethasone.Skeletal muscle cell line Hskm was maintained at 37oC (95%/5% air/CO 2 ) in αMEM/F12 supplemented with 200mM L-glutamine, 1% FBS, 1mg/ml EGF, 0.1 mg/mL βFGF, 100UI/mL insulin and 10mM dexamethasone.

    Article Title: Postbiotic <i>Parabacteroides Distasonis</i> Supplementation Enhances Intestinal and Skeletal Muscle Function in Aged Mice
    Article Snippet: Human colorectal cell line HCT116 (ATCC) was maintained at 37oC (95%/5% air/CO2) in DMEM media (GIBCO) supplemented with 10% (v/v) FBS.. Skeletal muscle cell line Hskm was maintained at 37oC (95%/5% air/CO2) in αMEM/F12 supplemented with 200mM Lglutamine, 1% FBS, 1mg/ml EGF, 0.1 mg/mL βFGF, 100UI/mL insulin and 10mM dexamethasone.Skeletal muscle cell line Hskm was maintained at 37oC (95%/5% air/CO2) in αMEM/F12 supplemented with 200mM Lglutamine, 1% FBS, 1mg/ml EGF, 0.1 mg/mL βFGF, 100UI/mL insulin and 10mM dexamethasone.

    Western Blot:

    Article Title: Postbiotic Parabacteroides Distasonis Supplementation Enhances Intestinal and Skeletal Muscle Function in Aged Mice
    Article Snippet: Human colorectal cell line HCT116 (ATCC) was maintained at 37oC (95%/5% air/CO 2 ) in DMEM media (GIBCO) supplemented with 10% (v/v) FBS.. Skeletal muscle cell line Hskm was maintained at 37oC (95%/5% air/CO 2 ) in αMEM/F12 supplemented with 200mM L-glutamine, 1% FBS, 1mg/ml EGF, 0.1 mg/mL βFGF, 100UI/mL insulin and 10mM dexamethasone.Skeletal muscle cell line Hskm was maintained at 37oC (95%/5% air/CO 2 ) in αMEM/F12 supplemented with 200mM L-glutamine, 1% FBS, 1mg/ml EGF, 0.1 mg/mL βFGF, 100UI/mL insulin and 10mM dexamethasone.

    Article Title: Postbiotic <i>Parabacteroides Distasonis</i> Supplementation Enhances Intestinal and Skeletal Muscle Function in Aged Mice
    Article Snippet: Human colorectal cell line HCT116 (ATCC) was maintained at 37oC (95%/5% air/CO2) in DMEM media (GIBCO) supplemented with 10% (v/v) FBS.. Skeletal muscle cell line Hskm was maintained at 37oC (95%/5% air/CO2) in αMEM/F12 supplemented with 200mM Lglutamine, 1% FBS, 1mg/ml EGF, 0.1 mg/mL βFGF, 100UI/mL insulin and 10mM dexamethasone.Skeletal muscle cell line Hskm was maintained at 37oC (95%/5% air/CO2) in αMEM/F12 supplemented with 200mM Lglutamine, 1% FBS, 1mg/ml EGF, 0.1 mg/mL βFGF, 100UI/mL insulin and 10mM dexamethasone.

    Control:

    Article Title: Postbiotic Parabacteroides Distasonis Supplementation Enhances Intestinal and Skeletal Muscle Function in Aged Mice
    Article Snippet: Human colorectal cell line HCT116 (ATCC) was maintained at 37oC (95%/5% air/CO 2 ) in DMEM media (GIBCO) supplemented with 10% (v/v) FBS.. Skeletal muscle cell line Hskm was maintained at 37oC (95%/5% air/CO 2 ) in αMEM/F12 supplemented with 200mM L-glutamine, 1% FBS, 1mg/ml EGF, 0.1 mg/mL βFGF, 100UI/mL insulin and 10mM dexamethasone.Skeletal muscle cell line Hskm was maintained at 37oC (95%/5% air/CO 2 ) in αMEM/F12 supplemented with 200mM L-glutamine, 1% FBS, 1mg/ml EGF, 0.1 mg/mL βFGF, 100UI/mL insulin and 10mM dexamethasone.

    Article Title: Postbiotic <i>Parabacteroides Distasonis</i> Supplementation Enhances Intestinal and Skeletal Muscle Function in Aged Mice
    Article Snippet: Human colorectal cell line HCT116 (ATCC) was maintained at 37oC (95%/5% air/CO2) in DMEM media (GIBCO) supplemented with 10% (v/v) FBS.. Skeletal muscle cell line Hskm was maintained at 37oC (95%/5% air/CO2) in αMEM/F12 supplemented with 200mM Lglutamine, 1% FBS, 1mg/ml EGF, 0.1 mg/mL βFGF, 100UI/mL insulin and 10mM dexamethasone.Skeletal muscle cell line Hskm was maintained at 37oC (95%/5% air/CO2) in αMEM/F12 supplemented with 200mM Lglutamine, 1% FBS, 1mg/ml EGF, 0.1 mg/mL βFGF, 100UI/mL insulin and 10mM dexamethasone.

    Membrane:

    Article Title: Postbiotic Parabacteroides Distasonis Supplementation Enhances Intestinal and Skeletal Muscle Function in Aged Mice
    Article Snippet: Human colorectal cell line HCT116 (ATCC) was maintained at 37oC (95%/5% air/CO 2 ) in DMEM media (GIBCO) supplemented with 10% (v/v) FBS.. Skeletal muscle cell line Hskm was maintained at 37oC (95%/5% air/CO 2 ) in αMEM/F12 supplemented with 200mM L-glutamine, 1% FBS, 1mg/ml EGF, 0.1 mg/mL βFGF, 100UI/mL insulin and 10mM dexamethasone.Skeletal muscle cell line Hskm was maintained at 37oC (95%/5% air/CO 2 ) in αMEM/F12 supplemented with 200mM L-glutamine, 1% FBS, 1mg/ml EGF, 0.1 mg/mL βFGF, 100UI/mL insulin and 10mM dexamethasone.

    Article Title: Postbiotic <i>Parabacteroides Distasonis</i> Supplementation Enhances Intestinal and Skeletal Muscle Function in Aged Mice
    Article Snippet: Human colorectal cell line HCT116 (ATCC) was maintained at 37oC (95%/5% air/CO2) in DMEM media (GIBCO) supplemented with 10% (v/v) FBS.. Skeletal muscle cell line Hskm was maintained at 37oC (95%/5% air/CO2) in αMEM/F12 supplemented with 200mM Lglutamine, 1% FBS, 1mg/ml EGF, 0.1 mg/mL βFGF, 100UI/mL insulin and 10mM dexamethasone.Skeletal muscle cell line Hskm was maintained at 37oC (95%/5% air/CO2) in αMEM/F12 supplemented with 200mM Lglutamine, 1% FBS, 1mg/ml EGF, 0.1 mg/mL βFGF, 100UI/mL insulin and 10mM dexamethasone.



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    ATCC human colorectal cancer cell line hct116
    HADH-S is decreased in human colorectal cancer tissue (A) Immunofluorescence analysis of endogenous HADH expression using anti-HADH antibody in RKO and <t>HCT116</t> cells. Scale bars, 10 μm. (B) Immunoblotting assessment of nuclear, cytosolic, and mitochondrial fractions of RKO and HCT116 cells. (C) The expression of HADH in different grade CRC tumors from the TCGA database. (D) Kaplan-Meier curves depict the overall survival rate in patients with colon cancer with high or low expression of HADH from the TCGA database. (E) Representative IHC staining of HADH in colorectal cancer tissues and para-cancer tissues. Scale bars, 50 μm. The red arrows indicate nuclear staining of HADH. (F) Comparison of HADH IRS in CRC tissues and paired para-cancer tissues (mean ± SD; two-tailed one-way analysis of variance). (G) Nuclear staining of HADH in CRC tissues and paired para-cancer tissues (mean ± SD; ∗ p < 0.05; two-tailed t test).
    Human Colorectal Cancer Cell Line Hct116, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+colorectal+cell+line+hct116/HCT+116/pmc12860641-243-0-12
    Average 99 stars, based on 1 article reviews
    human colorectal cancer cell line hct116 - by Bioz Stars, 2026-09
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    human colorectal adenocarcinoma cell line hct116  (ATCC)
    99
    ATCC human colorectal adenocarcinoma cell line hct116
    HADH-S is decreased in human colorectal cancer tissue (A) Immunofluorescence analysis of endogenous HADH expression using anti-HADH antibody in RKO and <t>HCT116</t> cells. Scale bars, 10 μm. (B) Immunoblotting assessment of nuclear, cytosolic, and mitochondrial fractions of RKO and HCT116 cells. (C) The expression of HADH in different grade CRC tumors from the TCGA database. (D) Kaplan-Meier curves depict the overall survival rate in patients with colon cancer with high or low expression of HADH from the TCGA database. (E) Representative IHC staining of HADH in colorectal cancer tissues and para-cancer tissues. Scale bars, 50 μm. The red arrows indicate nuclear staining of HADH. (F) Comparison of HADH IRS in CRC tissues and paired para-cancer tissues (mean ± SD; two-tailed one-way analysis of variance). (G) Nuclear staining of HADH in CRC tissues and paired para-cancer tissues (mean ± SD; ∗ p < 0.05; two-tailed t test).
    Human Colorectal Adenocarcinoma Cell Line Hct116, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+colorectal+cell+line+hct116/HCT+116/pm41674488-47-81-102
    Average 99 stars, based on 1 article reviews
    human colorectal adenocarcinoma cell line hct116 - by Bioz Stars, 2026-09
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    Image Search Results


    Postbiotic Pd modifies mitochondria in a colon cell line. (A) Right panel-representative images of HCT116 treated or not with postbiotic Pd for 24h and labeled with TMRE to determine mitochondrial morphology. Bar = 10 µm. Left panel- bar graphs of the mitochondrial length analysis. Data are expressed as MEAN ± SEM of five independent experiments ****p≤0.0001. Mann-Whitney test . (B) Upper panel- representative Western blot of PGC1α and GADPH as a loading control in HCT116 cells treated or not with postbiotic Pd. Bottom panel- Bar graphs represent quantification of PGC1α/GADPH expressed as MEAN ± SEM of five independent experiments. ∗p < 0.05. Mann-Whitney test . (C) Upper panel- representative Seahorse trace of HCT116 cells treated or not with postbiotic Pd. A; oligomycin (1 µM), B;FCCP (250 µM), C; rotenone plus antimycin A (1 µM each). Bottom panel- basal and maximum OCR of HCT116 cells treated or not with postbiotic Pd. MEAN ± SEM of three independent experiments with 10 replicates each. ***P < 0.001 compared to control. Mann-Whitney test. (D) Upper panel- representative Western blot of CHOP and β-actin as a loading control in HCT116 cells treated or not with postbiotic Pd. Bottom panel- bar graphs represent quantification of CHOP/β-actin expressed as MEAN ± SEM of 3 independent experiments. ∗p < 0.05. Mann-Whitney test . (E) Upper panel- representative Western blot of VDAC1 and β-actin as a loading control in colon mucosa samples from 26-months-old mice treated or not with postbiotic Pd. Bottom panel- bar graphs represent quantification of VDAC1/β-actin expressed as MEAN ± SEM. Note that β-actin blot in is the same as in this figure, as the same membrane was stripped and re-probed for VDAC1. N = 3 in the control group and 4 for the Pd treated group. ∗p < 0.05. Mann-Whitney test .

    Journal: Aging and Disease

    Article Title: Postbiotic Parabacteroides Distasonis Supplementation Enhances Intestinal and Skeletal Muscle Function in Aged Mice

    doi: 10.14336/AD.2025.0188

    Figure Lengend Snippet: Postbiotic Pd modifies mitochondria in a colon cell line. (A) Right panel-representative images of HCT116 treated or not with postbiotic Pd for 24h and labeled with TMRE to determine mitochondrial morphology. Bar = 10 µm. Left panel- bar graphs of the mitochondrial length analysis. Data are expressed as MEAN ± SEM of five independent experiments ****p≤0.0001. Mann-Whitney test . (B) Upper panel- representative Western blot of PGC1α and GADPH as a loading control in HCT116 cells treated or not with postbiotic Pd. Bottom panel- Bar graphs represent quantification of PGC1α/GADPH expressed as MEAN ± SEM of five independent experiments. ∗p < 0.05. Mann-Whitney test . (C) Upper panel- representative Seahorse trace of HCT116 cells treated or not with postbiotic Pd. A; oligomycin (1 µM), B;FCCP (250 µM), C; rotenone plus antimycin A (1 µM each). Bottom panel- basal and maximum OCR of HCT116 cells treated or not with postbiotic Pd. MEAN ± SEM of three independent experiments with 10 replicates each. ***P < 0.001 compared to control. Mann-Whitney test. (D) Upper panel- representative Western blot of CHOP and β-actin as a loading control in HCT116 cells treated or not with postbiotic Pd. Bottom panel- bar graphs represent quantification of CHOP/β-actin expressed as MEAN ± SEM of 3 independent experiments. ∗p < 0.05. Mann-Whitney test . (E) Upper panel- representative Western blot of VDAC1 and β-actin as a loading control in colon mucosa samples from 26-months-old mice treated or not with postbiotic Pd. Bottom panel- bar graphs represent quantification of VDAC1/β-actin expressed as MEAN ± SEM. Note that β-actin blot in is the same as in this figure, as the same membrane was stripped and re-probed for VDAC1. N = 3 in the control group and 4 for the Pd treated group. ∗p < 0.05. Mann-Whitney test .

    Article Snippet: Human colorectal cell line HCT116 (ATCC) was maintained at 37oC (95%/5% air/CO 2 ) in DMEM media (GIBCO) supplemented with 10% (v/v) FBS.

    Techniques: Labeling, MANN-WHITNEY, Western Blot, Control, Membrane

    (A) Schematic representation of the concept of immune checkpoint inhibition. Interaction between PD-1 and PD-L1 is blocked by Nivolumab which restores release of cytotoxic molecules by the CAR T cell (red) (B) Heatmap showing an overview of changes in tumor area and release of Granzyme B, IL-6, sPD-L1 and TNFα in HT-29-GFP and HCT116-GFP co-cultures in response to both single and combination treatments with Nivolumab, Ipilimumab and Temozolomide. Data used to generate the heatmap can be found in supplementary figures 7 and 8. (C,D) PCA plots showing response of HT-29-GFP and HCT116-GFP co-cultures to EpCAM-CD28 CAR T cells and treatments. (E) PCA plot showing the response of HT-29-GFP and HCT116-GFP co-cultures to combination treatments. Datapoints are scaled for the initial tumor cell density at the start of the co-culture. Pink circle indicates a small cluster of replicates consisting of HCT116-GFP cultures exposed to Nivolumab, Ipilimumab and Temozolomide. (F) Contribution and directionality of the different features of the principal components. (G) Heatmap showing morphometric parameters measured in the endothelial vessels of HT-29-GFP and HCT116-GFP co-cultures exposed to EpCAM-CD28 CART cells and treatments. Shown are fold changes against untreated controls. (H) Correlation distance matrix showing similarity between treatment responses based on patterns in relative change in tumor area, cytokine release and endothelial response. Data are presented as unsquared correlation distances, with values <1 indicating similarity in response while values >1 indicate distinct responses. A value of 1 means no relation between observed responses and a value of 0 indicates an identical response.

    Journal: bioRxiv

    Article Title: A scalable tumor-vasculature-on-chip for CAR T cell trafficking and efficacy studies

    doi: 10.64898/2026.02.05.703975

    Figure Lengend Snippet: (A) Schematic representation of the concept of immune checkpoint inhibition. Interaction between PD-1 and PD-L1 is blocked by Nivolumab which restores release of cytotoxic molecules by the CAR T cell (red) (B) Heatmap showing an overview of changes in tumor area and release of Granzyme B, IL-6, sPD-L1 and TNFα in HT-29-GFP and HCT116-GFP co-cultures in response to both single and combination treatments with Nivolumab, Ipilimumab and Temozolomide. Data used to generate the heatmap can be found in supplementary figures 7 and 8. (C,D) PCA plots showing response of HT-29-GFP and HCT116-GFP co-cultures to EpCAM-CD28 CAR T cells and treatments. (E) PCA plot showing the response of HT-29-GFP and HCT116-GFP co-cultures to combination treatments. Datapoints are scaled for the initial tumor cell density at the start of the co-culture. Pink circle indicates a small cluster of replicates consisting of HCT116-GFP cultures exposed to Nivolumab, Ipilimumab and Temozolomide. (F) Contribution and directionality of the different features of the principal components. (G) Heatmap showing morphometric parameters measured in the endothelial vessels of HT-29-GFP and HCT116-GFP co-cultures exposed to EpCAM-CD28 CART cells and treatments. Shown are fold changes against untreated controls. (H) Correlation distance matrix showing similarity between treatment responses based on patterns in relative change in tumor area, cytokine release and endothelial response. Data are presented as unsquared correlation distances, with values <1 indicating similarity in response while values >1 indicate distinct responses. A value of 1 means no relation between observed responses and a value of 0 indicates an identical response.

    Article Snippet: Human colorectal cancer cell line HCT116-GFP (GeneCopoeia, SL024) was cultured in RPMI-1640 (Gibco, 11875093) supplemented with 10% Fetal Bovine Serum and 1 % Penicillin-Streptomycin.

    Techniques: Inhibition, Co-Culture Assay

    (A) HCT116-GFP tumor cells proliferate after introduction in the lumenised ECM and cause regression of the endothelial vessel over time. The fluorescent signal could be used to create a binary mask that was used to track growth of HCT116-GFP tumor cells from day 5 until day 8. Fluorescent area at each timepoint was normalized against the area at t=1 for each individual replicate (n=15). (B) Effect of treatments on HT-29-GFP tumor area. Data was normalized against the untreated control at each timepoint (n=8-16). (C) Effect of treatments on HCT116-GFP tumor area. Data was normalized against the untreated control at each timepoint (n=8-14). Data included in the graphs are presented as mean ± SD.

    Journal: bioRxiv

    Article Title: A scalable tumor-vasculature-on-chip for CAR T cell trafficking and efficacy studies

    doi: 10.64898/2026.02.05.703975

    Figure Lengend Snippet: (A) HCT116-GFP tumor cells proliferate after introduction in the lumenised ECM and cause regression of the endothelial vessel over time. The fluorescent signal could be used to create a binary mask that was used to track growth of HCT116-GFP tumor cells from day 5 until day 8. Fluorescent area at each timepoint was normalized against the area at t=1 for each individual replicate (n=15). (B) Effect of treatments on HT-29-GFP tumor area. Data was normalized against the untreated control at each timepoint (n=8-16). (C) Effect of treatments on HCT116-GFP tumor area. Data was normalized against the untreated control at each timepoint (n=8-14). Data included in the graphs are presented as mean ± SD.

    Article Snippet: Human colorectal cancer cell line HCT116-GFP (GeneCopoeia, SL024) was cultured in RPMI-1640 (Gibco, 11875093) supplemented with 10% Fetal Bovine Serum and 1 % Penicillin-Streptomycin.

    Techniques: Control

    (A) Analysis of cytokine levels (pg/mL) in media samples after 72 hours of co-culture of HT-29-GFP and HCT116-GFP tumor cells with EpCAM-CD28 CAR T cells. Co-cultures were untreated or exposed to Nivolumab, Ipilimumab and/or Temozolomide (n=8-14). (B) Cytokine levels in panel A were normalized against untreated controls per experiment resulting in fold changes that were used for principal component analysis (n=8-14). Data included in the graphs are presented as mean ± SD.

    Journal: bioRxiv

    Article Title: A scalable tumor-vasculature-on-chip for CAR T cell trafficking and efficacy studies

    doi: 10.64898/2026.02.05.703975

    Figure Lengend Snippet: (A) Analysis of cytokine levels (pg/mL) in media samples after 72 hours of co-culture of HT-29-GFP and HCT116-GFP tumor cells with EpCAM-CD28 CAR T cells. Co-cultures were untreated or exposed to Nivolumab, Ipilimumab and/or Temozolomide (n=8-14). (B) Cytokine levels in panel A were normalized against untreated controls per experiment resulting in fold changes that were used for principal component analysis (n=8-14). Data included in the graphs are presented as mean ± SD.

    Article Snippet: Human colorectal cancer cell line HCT116-GFP (GeneCopoeia, SL024) was cultured in RPMI-1640 (Gibco, 11875093) supplemented with 10% Fetal Bovine Serum and 1 % Penicillin-Streptomycin.

    Techniques: Co-Culture Assay

    (A) Endothelial vessels were co-cultured with either HT-29-GFP or HCT116-GFP tumor cells and stained with VE-cadherin after the 72-hour co-culture. Co-cultures were either untreated or exposed to single or combination treatments with Nivolumab, Ipilimumab and Temozolomide in the presence of EpCAM-CD28 CAR T cells (E:T = 1:1). The endothelial response was assessed by analysis of VE-cadherin objects using a range of different morphological and spatial descriptors using IN Carta® (n=7-14) and normalization against respective untreated controls containing CAR T cells for each parameter. Data are presented as mean ± SD. (B) Heatmap showing change in morphometric parameters measured in endothelial vessels, co-cultured with either HT-29-GFP or HCT116-GFP tumor cells, upon addition of EpCAM-CD28 CAR T cells (E:T = 1:1). Data is presented as fold changes against respective controls without CAR T cells.

    Journal: bioRxiv

    Article Title: A scalable tumor-vasculature-on-chip for CAR T cell trafficking and efficacy studies

    doi: 10.64898/2026.02.05.703975

    Figure Lengend Snippet: (A) Endothelial vessels were co-cultured with either HT-29-GFP or HCT116-GFP tumor cells and stained with VE-cadherin after the 72-hour co-culture. Co-cultures were either untreated or exposed to single or combination treatments with Nivolumab, Ipilimumab and Temozolomide in the presence of EpCAM-CD28 CAR T cells (E:T = 1:1). The endothelial response was assessed by analysis of VE-cadherin objects using a range of different morphological and spatial descriptors using IN Carta® (n=7-14) and normalization against respective untreated controls containing CAR T cells for each parameter. Data are presented as mean ± SD. (B) Heatmap showing change in morphometric parameters measured in endothelial vessels, co-cultured with either HT-29-GFP or HCT116-GFP tumor cells, upon addition of EpCAM-CD28 CAR T cells (E:T = 1:1). Data is presented as fold changes against respective controls without CAR T cells.

    Article Snippet: Human colorectal cancer cell line HCT116-GFP (GeneCopoeia, SL024) was cultured in RPMI-1640 (Gibco, 11875093) supplemented with 10% Fetal Bovine Serum and 1 % Penicillin-Streptomycin.

    Techniques: Cell Culture, Staining, Co-Culture Assay

    ALO induced inhibition of CRC cell proliferation and apoptosis After treating HCT116 and SW480 cells with different concentrations of ALO for 24 hours, cell viability ( A ) was detected by CCK-8; After HCT116 and SW480 cells were treated with 0 µM, 200 µM and 300 µM ALO for 24 hours, apoptosis ( B and C ) was detected by double staining with FITC and PI.The data were expressed as mean ± SD (n = 3). * p < 0.05, compared with the control group (0 µM); # p < 0.05, compared with the 200 µM treatment group.

    Journal: OncoTargets and Therapy

    Article Title: Aloperine Induces Ferroptosis of Colorectal Cancer Cells via the Nrf2 Pathway

    doi: 10.2147/OTT.S575500

    Figure Lengend Snippet: ALO induced inhibition of CRC cell proliferation and apoptosis After treating HCT116 and SW480 cells with different concentrations of ALO for 24 hours, cell viability ( A ) was detected by CCK-8; After HCT116 and SW480 cells were treated with 0 µM, 200 µM and 300 µM ALO for 24 hours, apoptosis ( B and C ) was detected by double staining with FITC and PI.The data were expressed as mean ± SD (n = 3). * p < 0.05, compared with the control group (0 µM); # p < 0.05, compared with the 200 µM treatment group.

    Article Snippet: Human colorectal cancer HCT116 (CL-0096) cell line and SW480 (CL-0223) cell line were purchased from Wuhan Procell Life Science & Technology Co., Ltd. (China).

    Techniques: Inhibition, CCK-8 Assay, Double Staining, Control

    ALO induced ferroptosis in CRC cells After treatment with 0 μM, 200 μM and 300 μM ALO for 24 hours, the lipid peroxidation levels in HCT116 ( A ) and SW480 ( B ) cells were detected by the BODIPY C11 fluorescent probe. ( C and D ) Present the quantitative analysis of the corresponding fluorescence intensity ratios. ( E and F ) show the relative MDA contents in HCT116 and SW480 cells, respectively. ( G and H ) indicate the ferrous ion (Fe 2 ⁺) contents in HCT116 and SW480 cells, respectively. ( I and J ) display the GSH contents in HCT116 and SW480 cells, respectively. The data were expressed as mean ± SD (n = 3). * p < 0.05, compared with the control group (0 µM); # p < 0.05, compared with the 200 µM treatment group.

    Journal: OncoTargets and Therapy

    Article Title: Aloperine Induces Ferroptosis of Colorectal Cancer Cells via the Nrf2 Pathway

    doi: 10.2147/OTT.S575500

    Figure Lengend Snippet: ALO induced ferroptosis in CRC cells After treatment with 0 μM, 200 μM and 300 μM ALO for 24 hours, the lipid peroxidation levels in HCT116 ( A ) and SW480 ( B ) cells were detected by the BODIPY C11 fluorescent probe. ( C and D ) Present the quantitative analysis of the corresponding fluorescence intensity ratios. ( E and F ) show the relative MDA contents in HCT116 and SW480 cells, respectively. ( G and H ) indicate the ferrous ion (Fe 2 ⁺) contents in HCT116 and SW480 cells, respectively. ( I and J ) display the GSH contents in HCT116 and SW480 cells, respectively. The data were expressed as mean ± SD (n = 3). * p < 0.05, compared with the control group (0 µM); # p < 0.05, compared with the 200 µM treatment group.

    Article Snippet: Human colorectal cancer HCT116 (CL-0096) cell line and SW480 (CL-0223) cell line were purchased from Wuhan Procell Life Science & Technology Co., Ltd. (China).

    Techniques: Fluorescence, Control

    Iron Death Inhibitors DFO and Fer-1 reverse ALO-induced Ferroptosis After treating HCT116 and SW480 cells with DFO and Fer-1.Cell viability of HCT116 ( A ) and SW480 ( B ) cells in different groups was detected by CCK-8. Cell apoptosis changes in DFO ( C ) and Fer-1 ( D ) groups were detected by flow cytometry. ( E and F ) show the quantitative statistics of flow cytometry results. The data were expressed as mean ± SD (n = 3). * p < 0.05, compared with the control group; # p < 0.05, compared with the ALO-treated group.

    Journal: OncoTargets and Therapy

    Article Title: Aloperine Induces Ferroptosis of Colorectal Cancer Cells via the Nrf2 Pathway

    doi: 10.2147/OTT.S575500

    Figure Lengend Snippet: Iron Death Inhibitors DFO and Fer-1 reverse ALO-induced Ferroptosis After treating HCT116 and SW480 cells with DFO and Fer-1.Cell viability of HCT116 ( A ) and SW480 ( B ) cells in different groups was detected by CCK-8. Cell apoptosis changes in DFO ( C ) and Fer-1 ( D ) groups were detected by flow cytometry. ( E and F ) show the quantitative statistics of flow cytometry results. The data were expressed as mean ± SD (n = 3). * p < 0.05, compared with the control group; # p < 0.05, compared with the ALO-treated group.

    Article Snippet: Human colorectal cancer HCT116 (CL-0096) cell line and SW480 (CL-0223) cell line were purchased from Wuhan Procell Life Science & Technology Co., Ltd. (China).

    Techniques: CCK-8 Assay, Flow Cytometry, Control

    ALO induces mitochondrial apoptosis in CRC cells After treating HCT116 and SW480 cells with different concentrations of ALO (0 µM, 200 µM and 300 µM) for 24 hours, the ROS levels of the cells ( A – D ) were detected by flow cytometry. Western blotting was used to detect the protein expressions of Bcl-2, Bax and Caspase3 ( E – J ). The data were expressed as mean ± SD (n = 3). * p < 0.05, compared with the control group (0 µM); # p < 0.05, compared with the 200 µM treatment group.

    Journal: OncoTargets and Therapy

    Article Title: Aloperine Induces Ferroptosis of Colorectal Cancer Cells via the Nrf2 Pathway

    doi: 10.2147/OTT.S575500

    Figure Lengend Snippet: ALO induces mitochondrial apoptosis in CRC cells After treating HCT116 and SW480 cells with different concentrations of ALO (0 µM, 200 µM and 300 µM) for 24 hours, the ROS levels of the cells ( A – D ) were detected by flow cytometry. Western blotting was used to detect the protein expressions of Bcl-2, Bax and Caspase3 ( E – J ). The data were expressed as mean ± SD (n = 3). * p < 0.05, compared with the control group (0 µM); # p < 0.05, compared with the 200 µM treatment group.

    Article Snippet: Human colorectal cancer HCT116 (CL-0096) cell line and SW480 (CL-0223) cell line were purchased from Wuhan Procell Life Science & Technology Co., Ltd. (China).

    Techniques: Flow Cytometry, Western Blot, Control

    ALO induces ferroptosis in CRC cells by inhibiting the Nrf2 pathway The binding conformation between ALO and the Nrf2 receptor was analyzed using AutoDock Tools. The lowest binding energy conformation was identified at the ALA-510 binding site, which interacts via a hydrogen bond with a length of 1.9 ( A ). Potential active pockets of ALO in the Nrf2 protein were evaluated using CavityPlus software; the GLY364-ALA670 domain was identified as the active binding pocket of Nrf2, and ALO bound to this pocket as expected ( B ). After treating HCT116 and SW480 cells with ALO (0 µM, 200 µM and 300 µM) for 24 hours, immunofluorescence was used to detect intracellular Nrf2 changes in HCT116 ( C and D ) and SW480 ( E and F ) cells treated with different concentrations of ALO. Western Blotting was used to detect the protein expression levels of Nrf2, DMT1, xCT and GPX4 ( G – J ). The data were expressed as mean ± SD (n = 3). * p < 0.05, compared with the control group (0 µM); # p < 0.05, compared with the 200 µM treatment group.

    Journal: OncoTargets and Therapy

    Article Title: Aloperine Induces Ferroptosis of Colorectal Cancer Cells via the Nrf2 Pathway

    doi: 10.2147/OTT.S575500

    Figure Lengend Snippet: ALO induces ferroptosis in CRC cells by inhibiting the Nrf2 pathway The binding conformation between ALO and the Nrf2 receptor was analyzed using AutoDock Tools. The lowest binding energy conformation was identified at the ALA-510 binding site, which interacts via a hydrogen bond with a length of 1.9 ( A ). Potential active pockets of ALO in the Nrf2 protein were evaluated using CavityPlus software; the GLY364-ALA670 domain was identified as the active binding pocket of Nrf2, and ALO bound to this pocket as expected ( B ). After treating HCT116 and SW480 cells with ALO (0 µM, 200 µM and 300 µM) for 24 hours, immunofluorescence was used to detect intracellular Nrf2 changes in HCT116 ( C and D ) and SW480 ( E and F ) cells treated with different concentrations of ALO. Western Blotting was used to detect the protein expression levels of Nrf2, DMT1, xCT and GPX4 ( G – J ). The data were expressed as mean ± SD (n = 3). * p < 0.05, compared with the control group (0 µM); # p < 0.05, compared with the 200 µM treatment group.

    Article Snippet: Human colorectal cancer HCT116 (CL-0096) cell line and SW480 (CL-0223) cell line were purchased from Wuhan Procell Life Science & Technology Co., Ltd. (China).

    Techniques: Binding Assay, Software, Immunofluorescence, Western Blot, Expressing, Control

    Overexpression of Nrf2 inhibits ALO-induced ferroptosis HCT116 and SW480 cells were transfected with pcDNA3.1-Nrf2 plasmid; Nrf2 mRNA expression was detected by qRT-PCR ( A ), and Nrf2 protein expression by Western blotting ( B ). After 24 hours treatment of mock and Nrf2-overexpressing cells with ALO (300 µM), cell viability was measured by CCK-8 ( C ), and intracellular MDA ( D ), iron ( E ), GSH ( F ) levels were detected; intracellular ROS levels were analyzed by flow cytometry ( G ), and cell apoptosis was assessed by FITC-PI double staining ( H and I ). The data were expressed as mean ± SD (n = 3). * p < 0.05, compared with the mock group.

    Journal: OncoTargets and Therapy

    Article Title: Aloperine Induces Ferroptosis of Colorectal Cancer Cells via the Nrf2 Pathway

    doi: 10.2147/OTT.S575500

    Figure Lengend Snippet: Overexpression of Nrf2 inhibits ALO-induced ferroptosis HCT116 and SW480 cells were transfected with pcDNA3.1-Nrf2 plasmid; Nrf2 mRNA expression was detected by qRT-PCR ( A ), and Nrf2 protein expression by Western blotting ( B ). After 24 hours treatment of mock and Nrf2-overexpressing cells with ALO (300 µM), cell viability was measured by CCK-8 ( C ), and intracellular MDA ( D ), iron ( E ), GSH ( F ) levels were detected; intracellular ROS levels were analyzed by flow cytometry ( G ), and cell apoptosis was assessed by FITC-PI double staining ( H and I ). The data were expressed as mean ± SD (n = 3). * p < 0.05, compared with the mock group.

    Article Snippet: Human colorectal cancer HCT116 (CL-0096) cell line and SW480 (CL-0223) cell line were purchased from Wuhan Procell Life Science & Technology Co., Ltd. (China).

    Techniques: Over Expression, Transfection, Plasmid Preparation, Expressing, Quantitative RT-PCR, Western Blot, CCK-8 Assay, Flow Cytometry, Double Staining

    FFAR4 activator TUG891 reduces cell growth. ( A - B ) CCK-8 assays showing the effects of increasing concentrations of TUG891 (0–80 µM) on the proliferation of HCT116 and HT29 cells after 48 h. ( C ) Flow cytometric analysis of cell cycle distribution in HCT116 (upper panel) and HT29 (lower panel) cells following treatment with increasing concentrations of TUG891. ( D ) Western blot analysis of Cyclin D1 expression in CRC cells treated with 40 µM TUG891 in HCT116 (upper panel) and HT29 (lower panel) cells. ( E ) Flow cytometric analysis of apoptosis in CRC cells following TUG891 treatment, as assessed by Annexin V/PI staining. ( F ) Validation of FFAR4 knockdown efficiency at both the mRNA and protein levels. ( G ) CCK-8 assays assessing cell proliferation in control, FFAR4 knockdown, TUG891-treated, and combined FFAR4 knockdown plus TUG891 groups. ( H ) Cell cycle analysis showing the effects of FFAR4 knockdown on TUG891-induced G0/G1 phase arrest. Data are presented as the mean ± standard deviation (SD). Statistical significance was determined using one-way ANOVA followed by Tukey’s multiple comparisons tests. Exact P values are shown for significant differences. ns, not significant ( P ≥ 0.05)

    Journal: Journal of Translational Medicine

    Article Title: FFAR4 negatively regulates colorectal cancer growth via blocking oxidative phosphorylation

    doi: 10.1186/s12967-026-07942-4

    Figure Lengend Snippet: FFAR4 activator TUG891 reduces cell growth. ( A - B ) CCK-8 assays showing the effects of increasing concentrations of TUG891 (0–80 µM) on the proliferation of HCT116 and HT29 cells after 48 h. ( C ) Flow cytometric analysis of cell cycle distribution in HCT116 (upper panel) and HT29 (lower panel) cells following treatment with increasing concentrations of TUG891. ( D ) Western blot analysis of Cyclin D1 expression in CRC cells treated with 40 µM TUG891 in HCT116 (upper panel) and HT29 (lower panel) cells. ( E ) Flow cytometric analysis of apoptosis in CRC cells following TUG891 treatment, as assessed by Annexin V/PI staining. ( F ) Validation of FFAR4 knockdown efficiency at both the mRNA and protein levels. ( G ) CCK-8 assays assessing cell proliferation in control, FFAR4 knockdown, TUG891-treated, and combined FFAR4 knockdown plus TUG891 groups. ( H ) Cell cycle analysis showing the effects of FFAR4 knockdown on TUG891-induced G0/G1 phase arrest. Data are presented as the mean ± standard deviation (SD). Statistical significance was determined using one-way ANOVA followed by Tukey’s multiple comparisons tests. Exact P values are shown for significant differences. ns, not significant ( P ≥ 0.05)

    Article Snippet: Human colorectal cancer cell lines HCT116 (CCL-247EMT; ATCC) and HT29 (HTB-38; ATCC) were obtained from the Shanghai Institute of Cell Biology, Chinese Academy of Sciences, Shanghai, China.

    Techniques: CCK-8 Assay, Western Blot, Expressing, Staining, Biomarker Discovery, Knockdown, Control, Cell Cycle Assay, Standard Deviation

    FFAR4 activation promotes glycolysis and is associated with inhibition of oxidative phosphorylation. ( A ) Medium color shift observed in HCT116 cultures treated with increasing concentrations of TUG891. ( B ) TUG891-induced modulation of lactate secretion in HCT116 medium at 40 µM concentration. ( C ) Color shift in HT29 culture medium following treatment with increasing TUG891 concentrations. ( D ) Modulation of medium lactate content in HT29 cells following treatment with 40 µM TUG891. ( E ) Evaluation of TUG891-mediated antitumor effects in HCT116 (upper) and HT29 (lower) cells under pH-stabilized conditions achieved through NaHCO₃ addition or regular medium renewal. ( F ) Lactate metabolic pathway. ( G ) Effects of glucose supplementation on TUG891’s antitumor activity in HCT116 (left) and HT29 (right) cells. ( H ) Effect of 40 µM TUG891 on extracellular acidification rate (ECAR) in HCT116 (left) and HT29 (right) cells. ( I ) Impact of 40 µM TUG891 on oxygen consumption rate (OCR) in HCT116 (left) and HT29 (right) cells. Data are presented as mean ± standard deviation (SD). Statistical significance was determined using one-way ANOVA and Tukey’s multiple comparisons tests. ns, not significant ( P ≥ 0.05)

    Journal: Journal of Translational Medicine

    Article Title: FFAR4 negatively regulates colorectal cancer growth via blocking oxidative phosphorylation

    doi: 10.1186/s12967-026-07942-4

    Figure Lengend Snippet: FFAR4 activation promotes glycolysis and is associated with inhibition of oxidative phosphorylation. ( A ) Medium color shift observed in HCT116 cultures treated with increasing concentrations of TUG891. ( B ) TUG891-induced modulation of lactate secretion in HCT116 medium at 40 µM concentration. ( C ) Color shift in HT29 culture medium following treatment with increasing TUG891 concentrations. ( D ) Modulation of medium lactate content in HT29 cells following treatment with 40 µM TUG891. ( E ) Evaluation of TUG891-mediated antitumor effects in HCT116 (upper) and HT29 (lower) cells under pH-stabilized conditions achieved through NaHCO₃ addition or regular medium renewal. ( F ) Lactate metabolic pathway. ( G ) Effects of glucose supplementation on TUG891’s antitumor activity in HCT116 (left) and HT29 (right) cells. ( H ) Effect of 40 µM TUG891 on extracellular acidification rate (ECAR) in HCT116 (left) and HT29 (right) cells. ( I ) Impact of 40 µM TUG891 on oxygen consumption rate (OCR) in HCT116 (left) and HT29 (right) cells. Data are presented as mean ± standard deviation (SD). Statistical significance was determined using one-way ANOVA and Tukey’s multiple comparisons tests. ns, not significant ( P ≥ 0.05)

    Article Snippet: Human colorectal cancer cell lines HCT116 (CCL-247EMT; ATCC) and HT29 (HTB-38; ATCC) were obtained from the Shanghai Institute of Cell Biology, Chinese Academy of Sciences, Shanghai, China.

    Techniques: Activation Assay, Inhibition, Phospho-proteomics, Concentration Assay, Activity Assay, Standard Deviation

    TUG891 reduces the NAD⁺/NADH ratio and disrupts mitochondrial redox homeostasis. ( A - B ) Principal-component analysis (PCA) of gene expression data, showing the clustering of gene profiles for control and FFAR4 activation groups in HCT116 cells ( A ) and HT29 cells ( B ). ( C ) Changes in metabolite levels with and without TUG891 treatment in HCT116 cells (upper panel) and HT29 cells (lower panel). Log2(FC) indicates log2-transformed fold change of the TUG891-treated group relative to the control group. ( D - E ) Over-Representation Analysis identified significantly enriched KEGG pathways based on different metabolites in HCT116 cells ( D ) and HT29 cells ( E ). ( F ) Western blot analysis of malate–aspartate shuttle–related enzymes (GOT1, GOT2, MDH1, and MDH2) and OXPHOS proteins in control and TUG891-treated cells. ( G - H ) Measurement of NAD + levels and the NAD + /NADH ratio in HCT116 cells comparing vehicle and FFAR4 activator groups. ( I - J ) Measurement of NAD + levels and the NAD + /NADH ratio in HT29 cells comparing vehicle and FFAR4 activator groups. ( K , L ) Measurement of the cellular ATP/ADP ratio in HCT116 ( K ) and HT29 ( L ) cells comparing vehicle and FFAR4 activator–treated groups. The data were expressed as the mean ± standard deviation (SD)

    Journal: Journal of Translational Medicine

    Article Title: FFAR4 negatively regulates colorectal cancer growth via blocking oxidative phosphorylation

    doi: 10.1186/s12967-026-07942-4

    Figure Lengend Snippet: TUG891 reduces the NAD⁺/NADH ratio and disrupts mitochondrial redox homeostasis. ( A - B ) Principal-component analysis (PCA) of gene expression data, showing the clustering of gene profiles for control and FFAR4 activation groups in HCT116 cells ( A ) and HT29 cells ( B ). ( C ) Changes in metabolite levels with and without TUG891 treatment in HCT116 cells (upper panel) and HT29 cells (lower panel). Log2(FC) indicates log2-transformed fold change of the TUG891-treated group relative to the control group. ( D - E ) Over-Representation Analysis identified significantly enriched KEGG pathways based on different metabolites in HCT116 cells ( D ) and HT29 cells ( E ). ( F ) Western blot analysis of malate–aspartate shuttle–related enzymes (GOT1, GOT2, MDH1, and MDH2) and OXPHOS proteins in control and TUG891-treated cells. ( G - H ) Measurement of NAD + levels and the NAD + /NADH ratio in HCT116 cells comparing vehicle and FFAR4 activator groups. ( I - J ) Measurement of NAD + levels and the NAD + /NADH ratio in HT29 cells comparing vehicle and FFAR4 activator groups. ( K , L ) Measurement of the cellular ATP/ADP ratio in HCT116 ( K ) and HT29 ( L ) cells comparing vehicle and FFAR4 activator–treated groups. The data were expressed as the mean ± standard deviation (SD)

    Article Snippet: Human colorectal cancer cell lines HCT116 (CCL-247EMT; ATCC) and HT29 (HTB-38; ATCC) were obtained from the Shanghai Institute of Cell Biology, Chinese Academy of Sciences, Shanghai, China.

    Techniques: Gene Expression, Control, Activation Assay, Transformation Assay, Western Blot, Standard Deviation

    FMO3 knockdown suppresses migration, invasion, EMT, and PI3K/Akt signaling in CRC cells. (A–F) Reduced migration of HCT116 and HT29 cells after FMO3 knockdown. (G–L) Transwell assays show decreased migration and invasion. (M–P) EMT inhibition indicated by increased E-cadherin and reduced N-cadherin, Vimentin, and MMP2/9. (Q–T) Decreased PI3K and AKT phosphorylation following FMO3 silencing.

    Journal: Future Science OA

    Article Title: Targeting FMO3 suppresses the malignant phenotype of colorectal cancer: evidence from bioinformatics to functional experiments

    doi: 10.1080/20565623.2026.2629346

    Figure Lengend Snippet: FMO3 knockdown suppresses migration, invasion, EMT, and PI3K/Akt signaling in CRC cells. (A–F) Reduced migration of HCT116 and HT29 cells after FMO3 knockdown. (G–L) Transwell assays show decreased migration and invasion. (M–P) EMT inhibition indicated by increased E-cadherin and reduced N-cadherin, Vimentin, and MMP2/9. (Q–T) Decreased PI3K and AKT phosphorylation following FMO3 silencing.

    Article Snippet: Human colorectal cancer cell lines HCT116 and HT29 were purchased from Servicebio (Wuhan, China), and the normal colon epithelial cell line NCM460 from Zhongqiao Xinzhou Biotechnology (Shanghai, China).

    Techniques: Knockdown, Migration, Inhibition, Phospho-proteomics

    FMO3 knockdown induces G0/G1 arrest, inhibits colony formation, and alters cell-cycle and apoptosis-related proteins in CRC cells. (A–C, E–G) FMO3 knockdown increases G0/G1-phase and decreases S-phase cell populations. (D, H) CDK4 and CDK6 protein levels are reduced after FMO3 silencing. (I, J) Colony formation is significantly suppressed in HCT116 and HT29 cells. (K, L) Bax, P21, and P53 are upregulated, while Bcl-2 is decreased following FMO3 knockdown.

    Journal: Future Science OA

    Article Title: Targeting FMO3 suppresses the malignant phenotype of colorectal cancer: evidence from bioinformatics to functional experiments

    doi: 10.1080/20565623.2026.2629346

    Figure Lengend Snippet: FMO3 knockdown induces G0/G1 arrest, inhibits colony formation, and alters cell-cycle and apoptosis-related proteins in CRC cells. (A–C, E–G) FMO3 knockdown increases G0/G1-phase and decreases S-phase cell populations. (D, H) CDK4 and CDK6 protein levels are reduced after FMO3 silencing. (I, J) Colony formation is significantly suppressed in HCT116 and HT29 cells. (K, L) Bax, P21, and P53 are upregulated, while Bcl-2 is decreased following FMO3 knockdown.

    Article Snippet: Human colorectal cancer cell lines HCT116 and HT29 were purchased from Servicebio (Wuhan, China), and the normal colon epithelial cell line NCM460 from Zhongqiao Xinzhou Biotechnology (Shanghai, China).

    Techniques: Knockdown

    HADH-S is decreased in human colorectal cancer tissue (A) Immunofluorescence analysis of endogenous HADH expression using anti-HADH antibody in RKO and HCT116 cells. Scale bars, 10 μm. (B) Immunoblotting assessment of nuclear, cytosolic, and mitochondrial fractions of RKO and HCT116 cells. (C) The expression of HADH in different grade CRC tumors from the TCGA database. (D) Kaplan-Meier curves depict the overall survival rate in patients with colon cancer with high or low expression of HADH from the TCGA database. (E) Representative IHC staining of HADH in colorectal cancer tissues and para-cancer tissues. Scale bars, 50 μm. The red arrows indicate nuclear staining of HADH. (F) Comparison of HADH IRS in CRC tissues and paired para-cancer tissues (mean ± SD; two-tailed one-way analysis of variance). (G) Nuclear staining of HADH in CRC tissues and paired para-cancer tissues (mean ± SD; ∗ p < 0.05; two-tailed t test).

    Journal: iScience

    Article Title: A nuclear isoform of hydroxyacyl-COA dehydrogenase inhibits tumor progression in colorectal cancer

    doi: 10.1016/j.isci.2025.114470

    Figure Lengend Snippet: HADH-S is decreased in human colorectal cancer tissue (A) Immunofluorescence analysis of endogenous HADH expression using anti-HADH antibody in RKO and HCT116 cells. Scale bars, 10 μm. (B) Immunoblotting assessment of nuclear, cytosolic, and mitochondrial fractions of RKO and HCT116 cells. (C) The expression of HADH in different grade CRC tumors from the TCGA database. (D) Kaplan-Meier curves depict the overall survival rate in patients with colon cancer with high or low expression of HADH from the TCGA database. (E) Representative IHC staining of HADH in colorectal cancer tissues and para-cancer tissues. Scale bars, 50 μm. The red arrows indicate nuclear staining of HADH. (F) Comparison of HADH IRS in CRC tissues and paired para-cancer tissues (mean ± SD; two-tailed one-way analysis of variance). (G) Nuclear staining of HADH in CRC tissues and paired para-cancer tissues (mean ± SD; ∗ p < 0.05; two-tailed t test).

    Article Snippet: Human colorectal cancer cell line HCT116 and RKO were procured from the ATCC and maintained in DMEM medium (Gibco) supplemented with 10% fetal bovine serum at 37°C in a 5% CO 2 environment.

    Techniques: Immunofluorescence, Expressing, Western Blot, Immunohistochemistry, Staining, Comparison, Two Tailed Test

    HADH-S inhibits the tumorigenesis of colorectal cancer (A) The proliferation assay of RKO cells stably expressing HADH, HADH-L, or HADH-S. Cell number at day 4 was statistically analyzed. (B) EdU incorporation assay in RKO expressing HADH, HADH-L, or HADH-S. Scale bars, 20 μm. The analysis of EdU incorporation data is shown in the right panel. (C) Immunoblotting analysis of FLAG-tagged HADH, HADH-L, and HADH-S in HCT116 cells. (D) The proliferation assay of HCT116 cells expressing HADH, HADH-L, or HADH-S. Cell number at day 4 was statistically analyzed. (E) EdU incorporation assay in HCT116 expressing HADH, HADH-L, or HADH-S. (F) Immunoblotting analysis of HADH knockdown in HCT116 cells. (G) The proliferation assay of HCT116 cells with or without HADH knockdown. Cell number at day 4 was statistically analyzed. (H) EdU incorporation assay in HCT116 with or without HADH knockdown. (I) Colony formation assay of HCT116 cells expressing HADH, HADH-L, or HADH-S. The analysis is shown in the right panel. (J) The volume of xenograft tumors from mice implanted with the indicated HCT116 cells. (K) The images of xenograft tumors from mice implanted with the indicated HCT116 cells. The analysis of tumor weight is shown in the right panel. All the data are presented as mean ± SD. For panels G and H, a two-tailed t test was used. For panels A, B, D, E, I, J, and K, one-way ANOVA was used to compare multiple groups.∗ p < 0.05, ∗∗ p < 0.01, ns not significant.

    Journal: iScience

    Article Title: A nuclear isoform of hydroxyacyl-COA dehydrogenase inhibits tumor progression in colorectal cancer

    doi: 10.1016/j.isci.2025.114470

    Figure Lengend Snippet: HADH-S inhibits the tumorigenesis of colorectal cancer (A) The proliferation assay of RKO cells stably expressing HADH, HADH-L, or HADH-S. Cell number at day 4 was statistically analyzed. (B) EdU incorporation assay in RKO expressing HADH, HADH-L, or HADH-S. Scale bars, 20 μm. The analysis of EdU incorporation data is shown in the right panel. (C) Immunoblotting analysis of FLAG-tagged HADH, HADH-L, and HADH-S in HCT116 cells. (D) The proliferation assay of HCT116 cells expressing HADH, HADH-L, or HADH-S. Cell number at day 4 was statistically analyzed. (E) EdU incorporation assay in HCT116 expressing HADH, HADH-L, or HADH-S. (F) Immunoblotting analysis of HADH knockdown in HCT116 cells. (G) The proliferation assay of HCT116 cells with or without HADH knockdown. Cell number at day 4 was statistically analyzed. (H) EdU incorporation assay in HCT116 with or without HADH knockdown. (I) Colony formation assay of HCT116 cells expressing HADH, HADH-L, or HADH-S. The analysis is shown in the right panel. (J) The volume of xenograft tumors from mice implanted with the indicated HCT116 cells. (K) The images of xenograft tumors from mice implanted with the indicated HCT116 cells. The analysis of tumor weight is shown in the right panel. All the data are presented as mean ± SD. For panels G and H, a two-tailed t test was used. For panels A, B, D, E, I, J, and K, one-way ANOVA was used to compare multiple groups.∗ p < 0.05, ∗∗ p < 0.01, ns not significant.

    Article Snippet: Human colorectal cancer cell line HCT116 and RKO were procured from the ATCC and maintained in DMEM medium (Gibco) supplemented with 10% fetal bovine serum at 37°C in a 5% CO 2 environment.

    Techniques: Proliferation Assay, Stable Transfection, Expressing, Western Blot, Knockdown, Colony Assay, Two Tailed Test