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99
ATCC human colon cancer cell lines hct116
Tissue specification of neutrophils in the CRLM microenvironment. A, Expression levels of CXCR4, CXCR2, and CXCR1 across each TAN and PMN subset. B, mIHC staining of MPO, CXCR1, CXCR2, and CXCR4 in colorectal cancer and CRLM tissues. Scale bar, 50µm. C, Quantitative analysis of the percentage of CXCR1 + , CXCR2 + , and CXCR4 + neutrophils in paired colorectal cancer and CRLM tissues ( n = 5). D, Heatmap showing the mean strength of chemokine–receptor axis for each TAN subset in CRLM tissues. E, Predicted ordering of each TAN subset by CytoTRACE analysis using scRNA-seq dataset. F, Monocle 2 trajectory analysis of TAN subsets differentiation using the scRNA-seq dataset. Cells are colored by pseudotime, ordering predicted by CytoTRACE, and cell types. G, The density of each TAN subset along pseudotime. H, Clustering analysis of gene expression along pseudotime, with pathway enrichment analysis of four gene sets based on pseudotime. I, TAN1 similarity scores of TAN0_ELL2, TAN2_HSPA1B, TAN3_IFIT2, and TAN4_ARG1 across colorectal cancer, adjacent liver tissues (LP), and CRLM tissues. The TAN1 similarity score was calculated based on the top 50 differentially expressed genes in TAN1. J, Relative mRNA expression levels of BHLHE40 , CDKN1A (p21), LGALS3 , VEGFA , and LDHA as determined by qPCR in control neutrophils or neutrophils cocultured with <t>HCT116</t> or DLD-1 cells. K and L, Flow cytometry analysis of Gal3 surface expression in neutrophils cultured alone (control) or cocultured with DLD-1 ( K ) or HCT116 cells ( L ). P values were determined by paired Student t test ( C ) or unpaired Student t test ( J , K , and L ). n.s., not significant; **, P < 0.01; ***, P < 0.001. CRC, colorectal cancer; Ctrl, control; MFI, mean fluorescence intensity.
Human Colon Cancer Cell Lines 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/hct-116+colon+cancer+cell+line/HCT+116/pmc13628106-192-1-36
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human colon cancer cell lines hct116 - by Bioz Stars, 2026-10
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99
ATCC colon hct 116 cancer cell lines
Effect of the tested compounds on the cell viability of HCT 116, MCF-7 and NHDF cells. Cells were treated with different concentrations of BNAA hybrids for 24 h and then cell viability was measured by the CCK-8 assay. The results are provided as mean values with ±SD from at least three independent experiments. Cell viability was normalized to control (untreated) cells.
Colon Hct 116 Cancer Cell Lines, 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
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99
ATCC hct 116 colon cancer cell line
Combined histogram showing the IC 50 values of the Pd( ii ) complexes 4 and 5 against the MCF-7 <t>and</t> <t>HCT-116</t> cell lines.
Hct 116 Colon Cancer Cell Line, 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/hct-116+colon+cancer+cell+line/MCF7/pmc13126454-44-19-24
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ATCC hct 116 colon cancer cell lines
Combined histogram showing the IC 50 values of the Pd( ii ) complexes 4 and 5 against the MCF-7 <t>and</t> <t>HCT-116</t> cell lines.
Hct 116 Colon Cancer Cell Lines, 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/hct-116+colon+cancer+cell+line/HCT+116/pm41933767-157-1-7
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ATCC colorectal carcinoma colon cancer hct 116 cell line
Combined histogram showing the IC 50 values of the Pd( ii ) complexes 4 and 5 against the MCF-7 <t>and</t> <t>HCT-116</t> cell lines.
Colorectal Carcinoma Colon Cancer Hct 116 Cell Line, 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/hct-116+colon+cancer+cell+line/HCT+116/pmc12979646-57-1-11
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ATCC human cancer cell lines hela
Inhibiting PDH, GLS1 and Hsp90 by the combination of CPI‐613+BPTES+17‐AAG gave rise to enhanced senolysis on senescent fibroblasts as well as the therapy‐induced senescent tumor cells. (A, B) The effects of CPI‐613+BPTES+17‐AAG combination treatment on proliferating (A) and senescent (B) BJ cells. For the dose of each compound in use, see the results 2.7 section for more details. ** p < 0.01 by Student's t ‐test. (C, D) The effects of CPI‐613+BPTES+17‐AAG combination treatment on proliferating and Dox‐induced senescent lung <t>adenocarcinoma</t> <t>A549</t> cells. *** p < 0.001 by Student's t ‐test. (E, F) The effects of CPI‐613+BPTES+17‐AAG combination treatment on proliferating and Dox‐induced senescent cervical carcinoma <t>HeLa</t> cells. *** p < 0.001 by Student's t ‐test. (G) The morphological changes of senescent BJ induced by IR, senescent A549 and HeLa cells induced by Dox at the indicated time of CPI‐613+BPTES+17‐AAG treatment under the light microscopy. The senescent cells without treatment were stained with SA‐β‐gal. Cells were imaged at magnification 200×. (H) The schematic summarization of our findings. The activities of TCA cycle and chaperones are reduced in DNA damage induced senescent cells. Co‐inhibiting Hsp90 and TCA cycle with 17‐AAG+CPI‐613+BPTES combination leads to enhanced selective elimination of senescent cells, hinting TCA cycle and glutaminolysis are novel and potent targets for senolysis.
Human Cancer Cell Lines Hela, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


Tissue specification of neutrophils in the CRLM microenvironment. A, Expression levels of CXCR4, CXCR2, and CXCR1 across each TAN and PMN subset. B, mIHC staining of MPO, CXCR1, CXCR2, and CXCR4 in colorectal cancer and CRLM tissues. Scale bar, 50µm. C, Quantitative analysis of the percentage of CXCR1 + , CXCR2 + , and CXCR4 + neutrophils in paired colorectal cancer and CRLM tissues ( n = 5). D, Heatmap showing the mean strength of chemokine–receptor axis for each TAN subset in CRLM tissues. E, Predicted ordering of each TAN subset by CytoTRACE analysis using scRNA-seq dataset. F, Monocle 2 trajectory analysis of TAN subsets differentiation using the scRNA-seq dataset. Cells are colored by pseudotime, ordering predicted by CytoTRACE, and cell types. G, The density of each TAN subset along pseudotime. H, Clustering analysis of gene expression along pseudotime, with pathway enrichment analysis of four gene sets based on pseudotime. I, TAN1 similarity scores of TAN0_ELL2, TAN2_HSPA1B, TAN3_IFIT2, and TAN4_ARG1 across colorectal cancer, adjacent liver tissues (LP), and CRLM tissues. The TAN1 similarity score was calculated based on the top 50 differentially expressed genes in TAN1. J, Relative mRNA expression levels of BHLHE40 , CDKN1A (p21), LGALS3 , VEGFA , and LDHA as determined by qPCR in control neutrophils or neutrophils cocultured with HCT116 or DLD-1 cells. K and L, Flow cytometry analysis of Gal3 surface expression in neutrophils cultured alone (control) or cocultured with DLD-1 ( K ) or HCT116 cells ( L ). P values were determined by paired Student t test ( C ) or unpaired Student t test ( J , K , and L ). n.s., not significant; **, P < 0.01; ***, P < 0.001. CRC, colorectal cancer; Ctrl, control; MFI, mean fluorescence intensity.

Journal: Cancer Discovery

Article Title: Senescent-Like Neutrophils Shape Angiogenic Immunosuppressive Niches in Colorectal Cancer Liver Metastasis

doi: 10.1158/2159-8290.CD-25-0820

Figure Lengend Snippet: Tissue specification of neutrophils in the CRLM microenvironment. A, Expression levels of CXCR4, CXCR2, and CXCR1 across each TAN and PMN subset. B, mIHC staining of MPO, CXCR1, CXCR2, and CXCR4 in colorectal cancer and CRLM tissues. Scale bar, 50µm. C, Quantitative analysis of the percentage of CXCR1 + , CXCR2 + , and CXCR4 + neutrophils in paired colorectal cancer and CRLM tissues ( n = 5). D, Heatmap showing the mean strength of chemokine–receptor axis for each TAN subset in CRLM tissues. E, Predicted ordering of each TAN subset by CytoTRACE analysis using scRNA-seq dataset. F, Monocle 2 trajectory analysis of TAN subsets differentiation using the scRNA-seq dataset. Cells are colored by pseudotime, ordering predicted by CytoTRACE, and cell types. G, The density of each TAN subset along pseudotime. H, Clustering analysis of gene expression along pseudotime, with pathway enrichment analysis of four gene sets based on pseudotime. I, TAN1 similarity scores of TAN0_ELL2, TAN2_HSPA1B, TAN3_IFIT2, and TAN4_ARG1 across colorectal cancer, adjacent liver tissues (LP), and CRLM tissues. The TAN1 similarity score was calculated based on the top 50 differentially expressed genes in TAN1. J, Relative mRNA expression levels of BHLHE40 , CDKN1A (p21), LGALS3 , VEGFA , and LDHA as determined by qPCR in control neutrophils or neutrophils cocultured with HCT116 or DLD-1 cells. K and L, Flow cytometry analysis of Gal3 surface expression in neutrophils cultured alone (control) or cocultured with DLD-1 ( K ) or HCT116 cells ( L ). P values were determined by paired Student t test ( C ) or unpaired Student t test ( J , K , and L ). n.s., not significant; **, P < 0.01; ***, P < 0.001. CRC, colorectal cancer; Ctrl, control; MFI, mean fluorescence intensity.

Article Snippet: The human colon cancer cell lines HCT116 (RRID: CVCL_0291) and DLD-1 (RRID: CVCL_0248), mouse colon cancer cell line CT26 (RRID: CVCL_7254), as well as the human neutrophil cell line HL-60 (RRID: CVCL_0002) were obtained from the American Type Culture Collection.

Techniques: Tissue, Expressing, Staining, Analysis, Gene Expression, Control, Flow Cytometry, Cell Culture, Fluorescence

Effect of the tested compounds on the cell viability of HCT 116, MCF-7 and NHDF cells. Cells were treated with different concentrations of BNAA hybrids for 24 h and then cell viability was measured by the CCK-8 assay. The results are provided as mean values with ±SD from at least three independent experiments. Cell viability was normalized to control (untreated) cells.

Journal: International Journal of Molecular Sciences

Article Title: Betulin–Amino Acid Molecular Hybrids: Synthesis, Structure and Pharmacological Potential

doi: 10.3390/ijms27104445

Figure Lengend Snippet: Effect of the tested compounds on the cell viability of HCT 116, MCF-7 and NHDF cells. Cells were treated with different concentrations of BNAA hybrids for 24 h and then cell viability was measured by the CCK-8 assay. The results are provided as mean values with ±SD from at least three independent experiments. Cell viability was normalized to control (untreated) cells.

Article Snippet: Breast (MCF-7) and colon (HCT-116) cancer cell lines were obtained from ATCC (Manassas, VA, USA).

Techniques: CCK-8 Assay, Control

The relative expression levels of p21 and Bax in the HCT 116 cells treated with BNAA hybrids. Cells were treated with 100 µM BNAA hybrids for 24 h, after which the expression levels of p21 and Bax were measured using RT-qPCR. Relative quantification of the results was performed using the ΔΔCt method. Data is presented as the means of triplicate measurements ± SD.

Journal: International Journal of Molecular Sciences

Article Title: Betulin–Amino Acid Molecular Hybrids: Synthesis, Structure and Pharmacological Potential

doi: 10.3390/ijms27104445

Figure Lengend Snippet: The relative expression levels of p21 and Bax in the HCT 116 cells treated with BNAA hybrids. Cells were treated with 100 µM BNAA hybrids for 24 h, after which the expression levels of p21 and Bax were measured using RT-qPCR. Relative quantification of the results was performed using the ΔΔCt method. Data is presented as the means of triplicate measurements ± SD.

Article Snippet: Breast (MCF-7) and colon (HCT-116) cancer cell lines were obtained from ATCC (Manassas, VA, USA).

Techniques: Expressing, Quantitative RT-PCR, Quantitative Proteomics

Combined histogram showing the IC 50 values of the Pd( ii ) complexes 4 and 5 against the MCF-7 and HCT-116 cell lines.

Journal: RSC Advances

Article Title: Synthesis, structural characterization and molecular docking analysis of novel β-ketoiminato palladium( ii ) complexes with anticancer properties

doi: 10.1039/d5ra09325b

Figure Lengend Snippet: Combined histogram showing the IC 50 values of the Pd( ii ) complexes 4 and 5 against the MCF-7 and HCT-116 cell lines.

Article Snippet: Cancer cell lines were obtained from the ATCC (Manassas, VA), MCF7 human breast cancer cell line (ATCC® HTB-22TM, USA), HCT-116 colon cancer cell line (ATCC CCL-247TM, USA) and human skin fibroblast (ATCC® PCS-201-012TM).

Techniques:

Combined histogram displaying the binding energy scores of the Pd( ii ) complexes 4 and 5 against the KRAS-G13D, PIK3CA-H1047R and ATM-A112V targeted proteins in HCT-116.

Journal: RSC Advances

Article Title: Synthesis, structural characterization and molecular docking analysis of novel β-ketoiminato palladium( ii ) complexes with anticancer properties

doi: 10.1039/d5ra09325b

Figure Lengend Snippet: Combined histogram displaying the binding energy scores of the Pd( ii ) complexes 4 and 5 against the KRAS-G13D, PIK3CA-H1047R and ATM-A112V targeted proteins in HCT-116.

Article Snippet: Cancer cell lines were obtained from the ATCC (Manassas, VA), MCF7 human breast cancer cell line (ATCC® HTB-22TM, USA), HCT-116 colon cancer cell line (ATCC CCL-247TM, USA) and human skin fibroblast (ATCC® PCS-201-012TM).

Techniques: Binding Assay

Inhibiting PDH, GLS1 and Hsp90 by the combination of CPI‐613+BPTES+17‐AAG gave rise to enhanced senolysis on senescent fibroblasts as well as the therapy‐induced senescent tumor cells. (A, B) The effects of CPI‐613+BPTES+17‐AAG combination treatment on proliferating (A) and senescent (B) BJ cells. For the dose of each compound in use, see the results 2.7 section for more details. ** p < 0.01 by Student's t ‐test. (C, D) The effects of CPI‐613+BPTES+17‐AAG combination treatment on proliferating and Dox‐induced senescent lung adenocarcinoma A549 cells. *** p < 0.001 by Student's t ‐test. (E, F) The effects of CPI‐613+BPTES+17‐AAG combination treatment on proliferating and Dox‐induced senescent cervical carcinoma HeLa cells. *** p < 0.001 by Student's t ‐test. (G) The morphological changes of senescent BJ induced by IR, senescent A549 and HeLa cells induced by Dox at the indicated time of CPI‐613+BPTES+17‐AAG treatment under the light microscopy. The senescent cells without treatment were stained with SA‐β‐gal. Cells were imaged at magnification 200×. (H) The schematic summarization of our findings. The activities of TCA cycle and chaperones are reduced in DNA damage induced senescent cells. Co‐inhibiting Hsp90 and TCA cycle with 17‐AAG+CPI‐613+BPTES combination leads to enhanced selective elimination of senescent cells, hinting TCA cycle and glutaminolysis are novel and potent targets for senolysis.

Journal: Aging Cell

Article Title: Decreased Glucose Metabolism and Declined Chaperones Are Unique Features Required for the Survival of Senescent Fibroblasts and Pyruvate Dehydrogenase Is a Potent Senolytic Target

doi: 10.1111/acel.70434

Figure Lengend Snippet: Inhibiting PDH, GLS1 and Hsp90 by the combination of CPI‐613+BPTES+17‐AAG gave rise to enhanced senolysis on senescent fibroblasts as well as the therapy‐induced senescent tumor cells. (A, B) The effects of CPI‐613+BPTES+17‐AAG combination treatment on proliferating (A) and senescent (B) BJ cells. For the dose of each compound in use, see the results 2.7 section for more details. ** p < 0.01 by Student's t ‐test. (C, D) The effects of CPI‐613+BPTES+17‐AAG combination treatment on proliferating and Dox‐induced senescent lung adenocarcinoma A549 cells. *** p < 0.001 by Student's t ‐test. (E, F) The effects of CPI‐613+BPTES+17‐AAG combination treatment on proliferating and Dox‐induced senescent cervical carcinoma HeLa cells. *** p < 0.001 by Student's t ‐test. (G) The morphological changes of senescent BJ induced by IR, senescent A549 and HeLa cells induced by Dox at the indicated time of CPI‐613+BPTES+17‐AAG treatment under the light microscopy. The senescent cells without treatment were stained with SA‐β‐gal. Cells were imaged at magnification 200×. (H) The schematic summarization of our findings. The activities of TCA cycle and chaperones are reduced in DNA damage induced senescent cells. Co‐inhibiting Hsp90 and TCA cycle with 17‐AAG+CPI‐613+BPTES combination leads to enhanced selective elimination of senescent cells, hinting TCA cycle and glutaminolysis are novel and potent targets for senolysis.

Article Snippet: Human fibroblasts BJ (RRID: CVCL_3653; ATCC Cat#CRL‐2522), IMR‐90 (RRID: CVCL_0347; ATCC Cat#CCL‐186), WI‐38 (RRID: CVCL_0579; ATCC Cat#CCL‐75) and human cancer cell lines HeLa (RRID: CVCL_0030; ATCC Cat#CRM‐CCL‐2), A549 (RRID: CVCL_0023; ATCC Cat#CRM‐CCL‐185), and U2OS (RRID: CVCL_0042; ATCC Cat#HTB‐96) were purchased from American Type Culture Collection (ATCC) and cultured in Dulbecco's modified Eagle's medium (DMEM, Gibco) supplemented with 10% fetal bovine serum (FBS, Invitrogen) and 1% penicillin/streptomycin at 37°C under 5% CO 2 .

Techniques: Light Microscopy, Staining

Distinct proteomic and transcriptional signatures of metabolic enzymes and chaperones between senescent fibroblasts and the therapy‐induced senescent tumor cells. (A) The abundance of glycolysis‐related enzymes PFKP, ALDOA, PKM2, TCA cycle‐related PDHA, and glutaminolysis‐related GLS1 was decreased significantly in senescent BJ and IMR‐90 cells compared to their proliferating counterparts. (B) The protein levels of chaperones TCP1, Hsp70, and Hsp90 were decreased significantly in senescent BJ and IMR‐90 cells. (C) The abundance of those glycolysis‐related enzymes remained unchanged or even elevated in Dox‐induced senescent A549, HeLa, and U2OS tumor cells compared to their proliferating counterparts. (D) The abundance of these chaperone proteins in Dox‐induced senescent A549, HeLa, and U2OS tumor cells remained nearly unchanged. The relative abundance of each protein was quantified by signal density scanning on Western blots and normalized to the signal of β‐Actin or β‐tubulin. * p < 0.05, ** p < 0.01 tested by Student's t ‐test.

Journal: Aging Cell

Article Title: Decreased Glucose Metabolism and Declined Chaperones Are Unique Features Required for the Survival of Senescent Fibroblasts and Pyruvate Dehydrogenase Is a Potent Senolytic Target

doi: 10.1111/acel.70434

Figure Lengend Snippet: Distinct proteomic and transcriptional signatures of metabolic enzymes and chaperones between senescent fibroblasts and the therapy‐induced senescent tumor cells. (A) The abundance of glycolysis‐related enzymes PFKP, ALDOA, PKM2, TCA cycle‐related PDHA, and glutaminolysis‐related GLS1 was decreased significantly in senescent BJ and IMR‐90 cells compared to their proliferating counterparts. (B) The protein levels of chaperones TCP1, Hsp70, and Hsp90 were decreased significantly in senescent BJ and IMR‐90 cells. (C) The abundance of those glycolysis‐related enzymes remained unchanged or even elevated in Dox‐induced senescent A549, HeLa, and U2OS tumor cells compared to their proliferating counterparts. (D) The abundance of these chaperone proteins in Dox‐induced senescent A549, HeLa, and U2OS tumor cells remained nearly unchanged. The relative abundance of each protein was quantified by signal density scanning on Western blots and normalized to the signal of β‐Actin or β‐tubulin. * p < 0.05, ** p < 0.01 tested by Student's t ‐test.

Article Snippet: Human fibroblasts BJ (RRID: CVCL_3653; ATCC Cat#CRL‐2522), IMR‐90 (RRID: CVCL_0347; ATCC Cat#CCL‐186), WI‐38 (RRID: CVCL_0579; ATCC Cat#CCL‐75) and human cancer cell lines HeLa (RRID: CVCL_0030; ATCC Cat#CRM‐CCL‐2), A549 (RRID: CVCL_0023; ATCC Cat#CRM‐CCL‐185), and U2OS (RRID: CVCL_0042; ATCC Cat#HTB‐96) were purchased from American Type Culture Collection (ATCC) and cultured in Dulbecco's modified Eagle's medium (DMEM, Gibco) supplemented with 10% fetal bovine serum (FBS, Invitrogen) and 1% penicillin/streptomycin at 37°C under 5% CO 2 .

Techniques: Western Blot