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Procell Inc human normal colon epithelial cells
(A) Schematic of the experimental design. C57BL/6 mice were injected intraperitoneally with AOM to establish a CRC model and subsequently exposed to either fresh air or cigarette smoke for 2 h/day over 28 weeks. AOM (10 mg/kg) was administered once weekly for six consecutive weeks. Mice were sacrificed at week 28 (GF-AOM, n = 20; GF-AOMS, n = 20). (B) Tumor incidence in each group. (C) Representative images of colorectal tissues at the endpoint. (D) H&E staining of distal colorectal tissues showing <t>epithelial</t> hyperplasia and inflammatory infiltration; statistical analysis is shown (scale bar, 50 μm; magnification, 200×). (E) Immunohistochemical (IHC) staining of Ki67 in distal colorectal tissues; statistical analysis is shown (scale bar, 50 μm; magnification, 200×). Data are presented as mean ± SEM. Comparisons between two groups were performed using unpaired t-tests, and multiple group comparisons were performed using one-way ANOVA. ns, p > 0.05; *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001 .
Human Normal Colon Epithelial Cells, supplied by Procell Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/human normal colon epithelial cells/product/Procell Inc
Average 86 stars, based on 1 article reviews
human normal colon epithelial cells - by Bioz Stars, 2026-06
86/100 stars

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1) Product Images from "Cigarette smoke induces colon cancer by regulating the gut microbiota and related metabolites"

Article Title: Cigarette smoke induces colon cancer by regulating the gut microbiota and related metabolites

Journal: bioRxiv

doi: 10.64898/2026.01.30.702732

(A) Schematic of the experimental design. C57BL/6 mice were injected intraperitoneally with AOM to establish a CRC model and subsequently exposed to either fresh air or cigarette smoke for 2 h/day over 28 weeks. AOM (10 mg/kg) was administered once weekly for six consecutive weeks. Mice were sacrificed at week 28 (GF-AOM, n = 20; GF-AOMS, n = 20). (B) Tumor incidence in each group. (C) Representative images of colorectal tissues at the endpoint. (D) H&E staining of distal colorectal tissues showing epithelial hyperplasia and inflammatory infiltration; statistical analysis is shown (scale bar, 50 μm; magnification, 200×). (E) Immunohistochemical (IHC) staining of Ki67 in distal colorectal tissues; statistical analysis is shown (scale bar, 50 μm; magnification, 200×). Data are presented as mean ± SEM. Comparisons between two groups were performed using unpaired t-tests, and multiple group comparisons were performed using one-way ANOVA. ns, p > 0.05; *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001 .
Figure Legend Snippet: (A) Schematic of the experimental design. C57BL/6 mice were injected intraperitoneally with AOM to establish a CRC model and subsequently exposed to either fresh air or cigarette smoke for 2 h/day over 28 weeks. AOM (10 mg/kg) was administered once weekly for six consecutive weeks. Mice were sacrificed at week 28 (GF-AOM, n = 20; GF-AOMS, n = 20). (B) Tumor incidence in each group. (C) Representative images of colorectal tissues at the endpoint. (D) H&E staining of distal colorectal tissues showing epithelial hyperplasia and inflammatory infiltration; statistical analysis is shown (scale bar, 50 μm; magnification, 200×). (E) Immunohistochemical (IHC) staining of Ki67 in distal colorectal tissues; statistical analysis is shown (scale bar, 50 μm; magnification, 200×). Data are presented as mean ± SEM. Comparisons between two groups were performed using unpaired t-tests, and multiple group comparisons were performed using one-way ANOVA. ns, p > 0.05; *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001 .

Techniques Used: Injection, Staining, Immunohistochemical staining, Immunohistochemistry

A: qPCR analysis of CPT2 mRNA expression in colorectal cancer cell lines (SW480, HCT116, HT29) and normal human colon mucosal epithelial cells (NCM460). B: Western blot analysis of CPT2 protein expression in SW480, HCT116, HT29, and NCM460 cells, with β-actin as the loading control. C: qPCR validation of CPT2 knockdown efficiency in HT29 cells. D: Western blot validation of CPT2 knockdown efficiency in HT29 cells, with β-actin as the loading control. E: CCK8 assay for cell proliferation. F: Transwell migration assay to assess cell migratory capacity. G: Matrigel invasion assay to evaluate cell invasive capacity. H: Flow cytometry analysis of cell apoptosis. I: Flow cytometry analysis of cell cycle distribution. Control represents HT29 cells without transduction, sh-NC indicates cells transduced with scrambled control vector, and sh-CPT2 represents HT29 cells with stable CPT2 knockdown. Data are presented as mean ± SEM. Comparisons between two groups were performed using unpaired t-tests, and multiple group comparisons were analyzed by one-way ANOVA. Statistical significance: ns, p > 0.05; * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001 .
Figure Legend Snippet: A: qPCR analysis of CPT2 mRNA expression in colorectal cancer cell lines (SW480, HCT116, HT29) and normal human colon mucosal epithelial cells (NCM460). B: Western blot analysis of CPT2 protein expression in SW480, HCT116, HT29, and NCM460 cells, with β-actin as the loading control. C: qPCR validation of CPT2 knockdown efficiency in HT29 cells. D: Western blot validation of CPT2 knockdown efficiency in HT29 cells, with β-actin as the loading control. E: CCK8 assay for cell proliferation. F: Transwell migration assay to assess cell migratory capacity. G: Matrigel invasion assay to evaluate cell invasive capacity. H: Flow cytometry analysis of cell apoptosis. I: Flow cytometry analysis of cell cycle distribution. Control represents HT29 cells without transduction, sh-NC indicates cells transduced with scrambled control vector, and sh-CPT2 represents HT29 cells with stable CPT2 knockdown. Data are presented as mean ± SEM. Comparisons between two groups were performed using unpaired t-tests, and multiple group comparisons were analyzed by one-way ANOVA. Statistical significance: ns, p > 0.05; * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001 .

Techniques Used: Expressing, Western Blot, Control, Biomarker Discovery, Knockdown, CCK-8 Assay, Transwell Migration Assay, Invasion Assay, Flow Cytometry, Transduction, Plasmid Preparation



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(A) Schematic of the experimental design. C57BL/6 mice were injected intraperitoneally with AOM to establish a CRC model and subsequently exposed to either fresh air or cigarette smoke for 2 h/day over 28 weeks. AOM (10 mg/kg) was administered once weekly for six consecutive weeks. Mice were sacrificed at week 28 (GF-AOM, n = 20; GF-AOMS, n = 20). (B) Tumor incidence in each group. (C) Representative images of colorectal tissues at the endpoint. (D) H&E staining of distal colorectal tissues showing <t>epithelial</t> hyperplasia and inflammatory infiltration; statistical analysis is shown (scale bar, 50 μm; magnification, 200×). (E) Immunohistochemical (IHC) staining of Ki67 in distal colorectal tissues; statistical analysis is shown (scale bar, 50 μm; magnification, 200×). Data are presented as mean ± SEM. Comparisons between two groups were performed using unpaired t-tests, and multiple group comparisons were performed using one-way ANOVA. ns, p > 0.05; *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001 .
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(A) Schematic of the experimental design. C57BL/6 mice were injected intraperitoneally with AOM to establish a CRC model and subsequently exposed to either fresh air or cigarette smoke for 2 h/day over 28 weeks. AOM (10 mg/kg) was administered once weekly for six consecutive weeks. Mice were sacrificed at week 28 (GF-AOM, n = 20; GF-AOMS, n = 20). (B) Tumor incidence in each group. (C) Representative images of colorectal tissues at the endpoint. (D) H&E staining of distal colorectal tissues showing epithelial hyperplasia and inflammatory infiltration; statistical analysis is shown (scale bar, 50 μm; magnification, 200×). (E) Immunohistochemical (IHC) staining of Ki67 in distal colorectal tissues; statistical analysis is shown (scale bar, 50 μm; magnification, 200×). Data are presented as mean ± SEM. Comparisons between two groups were performed using unpaired t-tests, and multiple group comparisons were performed using one-way ANOVA. ns, p > 0.05; *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001 .

Journal: bioRxiv

Article Title: Cigarette smoke induces colon cancer by regulating the gut microbiota and related metabolites

doi: 10.64898/2026.01.30.702732

Figure Lengend Snippet: (A) Schematic of the experimental design. C57BL/6 mice were injected intraperitoneally with AOM to establish a CRC model and subsequently exposed to either fresh air or cigarette smoke for 2 h/day over 28 weeks. AOM (10 mg/kg) was administered once weekly for six consecutive weeks. Mice were sacrificed at week 28 (GF-AOM, n = 20; GF-AOMS, n = 20). (B) Tumor incidence in each group. (C) Representative images of colorectal tissues at the endpoint. (D) H&E staining of distal colorectal tissues showing epithelial hyperplasia and inflammatory infiltration; statistical analysis is shown (scale bar, 50 μm; magnification, 200×). (E) Immunohistochemical (IHC) staining of Ki67 in distal colorectal tissues; statistical analysis is shown (scale bar, 50 μm; magnification, 200×). Data are presented as mean ± SEM. Comparisons between two groups were performed using unpaired t-tests, and multiple group comparisons were performed using one-way ANOVA. ns, p > 0.05; *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001 .

Article Snippet: Human normal colon epithelial cells (NCM460) and colorectal cancer cells (HT29) were purchased from Auragene (Changsha, China), while HCT116 and SW480 colorectal cancer cells were obtained from Procell (Wuhan, China).

Techniques: Injection, Staining, Immunohistochemical staining, Immunohistochemistry

A: qPCR analysis of CPT2 mRNA expression in colorectal cancer cell lines (SW480, HCT116, HT29) and normal human colon mucosal epithelial cells (NCM460). B: Western blot analysis of CPT2 protein expression in SW480, HCT116, HT29, and NCM460 cells, with β-actin as the loading control. C: qPCR validation of CPT2 knockdown efficiency in HT29 cells. D: Western blot validation of CPT2 knockdown efficiency in HT29 cells, with β-actin as the loading control. E: CCK8 assay for cell proliferation. F: Transwell migration assay to assess cell migratory capacity. G: Matrigel invasion assay to evaluate cell invasive capacity. H: Flow cytometry analysis of cell apoptosis. I: Flow cytometry analysis of cell cycle distribution. Control represents HT29 cells without transduction, sh-NC indicates cells transduced with scrambled control vector, and sh-CPT2 represents HT29 cells with stable CPT2 knockdown. Data are presented as mean ± SEM. Comparisons between two groups were performed using unpaired t-tests, and multiple group comparisons were analyzed by one-way ANOVA. Statistical significance: ns, p > 0.05; * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001 .

Journal: bioRxiv

Article Title: Cigarette smoke induces colon cancer by regulating the gut microbiota and related metabolites

doi: 10.64898/2026.01.30.702732

Figure Lengend Snippet: A: qPCR analysis of CPT2 mRNA expression in colorectal cancer cell lines (SW480, HCT116, HT29) and normal human colon mucosal epithelial cells (NCM460). B: Western blot analysis of CPT2 protein expression in SW480, HCT116, HT29, and NCM460 cells, with β-actin as the loading control. C: qPCR validation of CPT2 knockdown efficiency in HT29 cells. D: Western blot validation of CPT2 knockdown efficiency in HT29 cells, with β-actin as the loading control. E: CCK8 assay for cell proliferation. F: Transwell migration assay to assess cell migratory capacity. G: Matrigel invasion assay to evaluate cell invasive capacity. H: Flow cytometry analysis of cell apoptosis. I: Flow cytometry analysis of cell cycle distribution. Control represents HT29 cells without transduction, sh-NC indicates cells transduced with scrambled control vector, and sh-CPT2 represents HT29 cells with stable CPT2 knockdown. Data are presented as mean ± SEM. Comparisons between two groups were performed using unpaired t-tests, and multiple group comparisons were analyzed by one-way ANOVA. Statistical significance: ns, p > 0.05; * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001 .

Article Snippet: Human normal colon epithelial cells (NCM460) and colorectal cancer cells (HT29) were purchased from Auragene (Changsha, China), while HCT116 and SW480 colorectal cancer cells were obtained from Procell (Wuhan, China).

Techniques: Expressing, Western Blot, Control, Biomarker Discovery, Knockdown, CCK-8 Assay, Transwell Migration Assay, Invasion Assay, Flow Cytometry, Transduction, Plasmid Preparation

Cytotoxic response and intracellular ROS levels induced by the multimodal hydrogel nanoplatform in CRC and normal colon cell models. (A) Dose–response curve of free 5-FU in HCT-116 cells after 48 h, determined by MTT assay and used to define the experimental IC₅₀. Cell viability was normalized to the Ctrl. For visualization on a logarithmic x-axis, the Ctrl condition is plotted at a nominal concentration of 0.1 µg mL⁻¹. (B–D) MTT-based cell viability after 48 h treatment in (B) HCT-116, (C) SW480, and (D) normal human colon epithelial NCM460 cells. Treatment groups include Ctrl, free 5-FU (5FU), non-targeted nanoparticles (NP), HA-targeted nanoparticles (tNP), blank hydrogel (Gel), hydrogel-loaded targeted nanoparticles (Gel-tNP), and Gel-tNP combined with near-infrared irradiation (NIR, 808 nm), X-ray irradiation (XR, 2 Gy), or both. All treatments were administered at an equivalent 5-FU concentration corresponding to the IC₅₀ determined in panel (A). (E) Intracellular ROS levels in HCT-116 cells measured after 48 h using CellROX™ Deep Red and expressed as fold change relative to Ctrl. Data are mean ± SD ( n = 3). Statistical significance was assessed by one-way ANOVA with multiple-comparisons post-hoc testing. Asterisks indicate comparisons vs. Ctrl (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001). Brackets indicate the specific intergroup comparisons shown (e.g., dual-modal vs. tri-modal where indicated). “ns” denotes not significant

Journal: Journal of Biological Engineering

Article Title: Hydrogel-mediated tri-modal nanoplatform for localized colorectal cancer therapy via smart chemo–photothermal–radiotherapy

doi: 10.1186/s13036-026-00633-0

Figure Lengend Snippet: Cytotoxic response and intracellular ROS levels induced by the multimodal hydrogel nanoplatform in CRC and normal colon cell models. (A) Dose–response curve of free 5-FU in HCT-116 cells after 48 h, determined by MTT assay and used to define the experimental IC₅₀. Cell viability was normalized to the Ctrl. For visualization on a logarithmic x-axis, the Ctrl condition is plotted at a nominal concentration of 0.1 µg mL⁻¹. (B–D) MTT-based cell viability after 48 h treatment in (B) HCT-116, (C) SW480, and (D) normal human colon epithelial NCM460 cells. Treatment groups include Ctrl, free 5-FU (5FU), non-targeted nanoparticles (NP), HA-targeted nanoparticles (tNP), blank hydrogel (Gel), hydrogel-loaded targeted nanoparticles (Gel-tNP), and Gel-tNP combined with near-infrared irradiation (NIR, 808 nm), X-ray irradiation (XR, 2 Gy), or both. All treatments were administered at an equivalent 5-FU concentration corresponding to the IC₅₀ determined in panel (A). (E) Intracellular ROS levels in HCT-116 cells measured after 48 h using CellROX™ Deep Red and expressed as fold change relative to Ctrl. Data are mean ± SD ( n = 3). Statistical significance was assessed by one-way ANOVA with multiple-comparisons post-hoc testing. Asterisks indicate comparisons vs. Ctrl (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001). Brackets indicate the specific intergroup comparisons shown (e.g., dual-modal vs. tri-modal where indicated). “ns” denotes not significant

Article Snippet: The cytotoxicity of all treatment groups was evaluated using an MTT assay in two CRC cell lines and one normal human colon epithelial cell model. HCT-116 human colorectal carcinoma cells (ATCC ® CCL-247TM, American Type Culture Collection, USA) and SW480 human colorectal adenocarcinoma cells (ATCC ® CCL-228TM, American Type Culture Collection, USA) were used as CRC models, and normal human colon epithelial cells NCM460 (NCM460DTM; INCELL Corporation LLC, San Antonio, TX, USA) were used to provide an initial in-vitro assessment of relative tolerance in non-malignant colon epithelium.

Techniques: MTT Assay, Concentration Assay, Irradiation