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colorectal cancer cell lines hct15  (ATCC)


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    ATCC colorectal cancer cell lines hct15
    Urolithin A suppresses CRC cell proliferation and enhances T-cell activation. (A) Dose–response curves of UA in <t>HCT15,</t> HCT116, MC38, NCM460 and MCEC cells at 48 h and 72 h, with corresponding IC 50 values. The selectivity index (SI = IC 50 normal / IC 50 cancer) is shown for each cell line; (B-C) Effects of increasing concentrations of UA on the viability of CTLL-2 cells and human CD8 + T cells (hCD8 + T) at 48 h; (D) Schematic illustration of T-cell and tumor cell co-culture in the presence of UA; (E-G) Cell viability assays demonstrating that combined treatment with UA (20 or 25 µM) and T cells more effectively suppresses the proliferation of HCT15, HCT116, and MC38 cells compared with UA or T-cell treatment alone; (H) Western blot analysis showing the effects of UA (15, 20 or 25 µM) on the phosphorylation levels of AKT and mTOR in HCT15, HCT116, and MC38 cells, as well as the regulation of p-FOXO1, TCF1, GZMB, and p-AKT in hCD8⁺ T cells and CTLL-2 cells. P < 0.05 was considered statistically significant (* P < 0.05, ** P < 0.01, *** P < 0.001).
    Colorectal Cancer Cell Lines Hct15, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1654 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/colorectal+cancer+cell+line+hct15/HCT-15/pmc13184318-17-3-44
    Average 97 stars, based on 1654 article reviews
    colorectal cancer cell lines hct15 - by Bioz Stars, 2026-10
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    1) Product Images from "Urolithin A blocks colorectal cancer progression by AKT1 inhibition–driven immune activation"

    Article Title: Urolithin A blocks colorectal cancer progression by AKT1 inhibition–driven immune activation

    Journal: Scientific Reports

    doi: 10.1038/s41598-026-45621-y

    Urolithin A suppresses CRC cell proliferation and enhances T-cell activation. (A) Dose–response curves of UA in HCT15, HCT116, MC38, NCM460 and MCEC cells at 48 h and 72 h, with corresponding IC 50 values. The selectivity index (SI = IC 50 normal / IC 50 cancer) is shown for each cell line; (B-C) Effects of increasing concentrations of UA on the viability of CTLL-2 cells and human CD8 + T cells (hCD8 + T) at 48 h; (D) Schematic illustration of T-cell and tumor cell co-culture in the presence of UA; (E-G) Cell viability assays demonstrating that combined treatment with UA (20 or 25 µM) and T cells more effectively suppresses the proliferation of HCT15, HCT116, and MC38 cells compared with UA or T-cell treatment alone; (H) Western blot analysis showing the effects of UA (15, 20 or 25 µM) on the phosphorylation levels of AKT and mTOR in HCT15, HCT116, and MC38 cells, as well as the regulation of p-FOXO1, TCF1, GZMB, and p-AKT in hCD8⁺ T cells and CTLL-2 cells. P < 0.05 was considered statistically significant (* P < 0.05, ** P < 0.01, *** P < 0.001).
    Figure Legend Snippet: Urolithin A suppresses CRC cell proliferation and enhances T-cell activation. (A) Dose–response curves of UA in HCT15, HCT116, MC38, NCM460 and MCEC cells at 48 h and 72 h, with corresponding IC 50 values. The selectivity index (SI = IC 50 normal / IC 50 cancer) is shown for each cell line; (B-C) Effects of increasing concentrations of UA on the viability of CTLL-2 cells and human CD8 + T cells (hCD8 + T) at 48 h; (D) Schematic illustration of T-cell and tumor cell co-culture in the presence of UA; (E-G) Cell viability assays demonstrating that combined treatment with UA (20 or 25 µM) and T cells more effectively suppresses the proliferation of HCT15, HCT116, and MC38 cells compared with UA or T-cell treatment alone; (H) Western blot analysis showing the effects of UA (15, 20 or 25 µM) on the phosphorylation levels of AKT and mTOR in HCT15, HCT116, and MC38 cells, as well as the regulation of p-FOXO1, TCF1, GZMB, and p-AKT in hCD8⁺ T cells and CTLL-2 cells. P < 0.05 was considered statistically significant (* P < 0.05, ** P < 0.01, *** P < 0.001).

    Techniques Used: Activation Assay, Co-Culture Assay, Western Blot, Phospho-proteomics

    Urolithin A suppresses CRC proliferation, migration, invasion, and enhances CD8⁺ T-cell infiltration. (A–B) Wound-healing assays and quantification showing that UA(20 μm) combined with lymphocytes (hCD8 + T cells or CTLL-2) markedly inhibits migration of HCT15, HCT116, and MC38 cells at 24 h and 48 h; (C–D) Transwell invasion and migration assays and quantification indicating that UA (20 μm) together with lymphocytes significantly reduces invasion index of HCT15, HCT116, and MC38 cells; (E)Schematic diagram of the MC38 orthotopic colorectal cancer mouse model and treatment regimen with UA (100 mg/kg/day); (F–G) Representative macroscopic images and tumor volume measurements demonstrating that UA treatment inhibits tumor growth; (H) Representative H&E staining of tumors from vehicle- and UA-treated mice; (I) Immunohistochemical staining of Ki67 showing decreased proliferation in UA-treated tumors; (J) Immunohistochemical staining of CD8 revealing enhanced CD8⁺ T-cell infiltration in UA-treated tumors; (K) Quantitative analysis showing that UA lowers the proliferation index and increases CD8⁺ T-cell infiltration in vivo . P < 0.05 was considered statistically significant (* P < 0.05, ** P < 0.01, *** P < 0.001).
    Figure Legend Snippet: Urolithin A suppresses CRC proliferation, migration, invasion, and enhances CD8⁺ T-cell infiltration. (A–B) Wound-healing assays and quantification showing that UA(20 μm) combined with lymphocytes (hCD8 + T cells or CTLL-2) markedly inhibits migration of HCT15, HCT116, and MC38 cells at 24 h and 48 h; (C–D) Transwell invasion and migration assays and quantification indicating that UA (20 μm) together with lymphocytes significantly reduces invasion index of HCT15, HCT116, and MC38 cells; (E)Schematic diagram of the MC38 orthotopic colorectal cancer mouse model and treatment regimen with UA (100 mg/kg/day); (F–G) Representative macroscopic images and tumor volume measurements demonstrating that UA treatment inhibits tumor growth; (H) Representative H&E staining of tumors from vehicle- and UA-treated mice; (I) Immunohistochemical staining of Ki67 showing decreased proliferation in UA-treated tumors; (J) Immunohistochemical staining of CD8 revealing enhanced CD8⁺ T-cell infiltration in UA-treated tumors; (K) Quantitative analysis showing that UA lowers the proliferation index and increases CD8⁺ T-cell infiltration in vivo . P < 0.05 was considered statistically significant (* P < 0.05, ** P < 0.01, *** P < 0.001).

    Techniques Used: Migration, Staining, Immunohistochemical staining, In Vivo

    Related Articles

    Cell Culture:

    Article Title: Combination of BEZ235 and Metformin Has Synergistic Effect on Cell Viability in Colorectal Cancer Cells
    Article Snippet: .. Reagents and cell culture The human colorectal cancer cell line HCT15 was purchased from American Type Culture Collection (Rockville, MD, USA). .. The cells were cultured in Dulbecco’s modified Eagle’s medium (DMEM) supplemented with 10% (vol/vol) heat inactivated fetal bovine serum (Gibco BRL, Rockville, MD, USA) and 1% streptomycin/penicillin at 37°C in a humidified atmosphere consisting of 5% CO2 and 95% air.

    Article Title: Blockage of Autophagy Rescues the Dual PI3K/mTOR Inhibitor BEZ235-induced Growth Inhibition of Colorectal Cancer Cells
    Article Snippet: .. Cell culture and reagents The human colorectal cancer cell line HCT15 was obtained from the American Type Culture Collection (Manassas, VA). .. Cells were grown in a monolayer culture in DMEM (Sigma) supplemented with 10% fetal bovine serum (Sigma) and 1% streptomycin/penicillin, and were maintained at 37°C in a humidified atmosphere consisting of 5% CO2 and 95% air.

    Article Title: Cathayanon E induces apoptosis and enhances oxaliplatin sensitivity in colorectal cancer through suppression of MCL1.
    Article Snippet: DMSO Dimethyl sulfoxide EdU 5-Ethynyl-2′-deoxyuridine GO Gene Ontology HRP Horseradish peroxidase IC50 Half-maximal inhibitory concentration KEGG Kyoto Encyclopedia of Genes and Genomes L-OHP Oxaliplatin MCL1 Myeloid cell leukemia 1 (anti-apoptotic protein) PPI Protein–protein interaction STRING Search Tool for the Retrieval of Interacting Genes/Proteins TUNEL Terminal deoxynucleotidyl transferase dUTP nick-end labeling β-TRCP Beta-transducin repeat–containing protein

    other:

    Article Title: Refractive Index Determination of Individual Viruses and Small Extracellular Vesicles in Aqueous Media Using Nano-Flow Cytometry.
    Article Snippet: The human colorectal cancer cell line (HCT15) was purchased from American Type Culture Collection (ATCC).



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    Urolithin A suppresses CRC cell proliferation and enhances T-cell activation. (A) Dose–response curves of UA in <t>HCT15,</t> HCT116, MC38, NCM460 and MCEC cells at 48 h and 72 h, with corresponding IC 50 values. The selectivity index (SI = IC 50 normal / IC 50 cancer) is shown for each cell line; (B-C) Effects of increasing concentrations of UA on the viability of CTLL-2 cells and human CD8 + T cells (hCD8 + T) at 48 h; (D) Schematic illustration of T-cell and tumor cell co-culture in the presence of UA; (E-G) Cell viability assays demonstrating that combined treatment with UA (20 or 25 µM) and T cells more effectively suppresses the proliferation of HCT15, HCT116, and MC38 cells compared with UA or T-cell treatment alone; (H) Western blot analysis showing the effects of UA (15, 20 or 25 µM) on the phosphorylation levels of AKT and mTOR in HCT15, HCT116, and MC38 cells, as well as the regulation of p-FOXO1, TCF1, GZMB, and p-AKT in hCD8⁺ T cells and CTLL-2 cells. P < 0.05 was considered statistically significant (* P < 0.05, ** P < 0.01, *** P < 0.001).
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    Urolithin A suppresses CRC cell proliferation and enhances T-cell activation. (A) Dose–response curves of UA in <t>HCT15,</t> HCT116, MC38, NCM460 and MCEC cells at 48 h and 72 h, with corresponding IC 50 values. The selectivity index (SI = IC 50 normal / IC 50 cancer) is shown for each cell line; (B-C) Effects of increasing concentrations of UA on the viability of CTLL-2 cells and human CD8 + T cells (hCD8 + T) at 48 h; (D) Schematic illustration of T-cell and tumor cell co-culture in the presence of UA; (E-G) Cell viability assays demonstrating that combined treatment with UA (20 or 25 µM) and T cells more effectively suppresses the proliferation of HCT15, HCT116, and MC38 cells compared with UA or T-cell treatment alone; (H) Western blot analysis showing the effects of UA (15, 20 or 25 µM) on the phosphorylation levels of AKT and mTOR in HCT15, HCT116, and MC38 cells, as well as the regulation of p-FOXO1, TCF1, GZMB, and p-AKT in hCD8⁺ T cells and CTLL-2 cells. P < 0.05 was considered statistically significant (* P < 0.05, ** P < 0.01, *** P < 0.001).
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    Urolithin A suppresses CRC cell proliferation and enhances T-cell activation. (A) Dose–response curves of UA in <t>HCT15,</t> HCT116, MC38, NCM460 and MCEC cells at 48 h and 72 h, with corresponding IC 50 values. The selectivity index (SI = IC 50 normal / IC 50 cancer) is shown for each cell line; (B-C) Effects of increasing concentrations of UA on the viability of CTLL-2 cells and human CD8 + T cells (hCD8 + T) at 48 h; (D) Schematic illustration of T-cell and tumor cell co-culture in the presence of UA; (E-G) Cell viability assays demonstrating that combined treatment with UA (20 or 25 µM) and T cells more effectively suppresses the proliferation of HCT15, HCT116, and MC38 cells compared with UA or T-cell treatment alone; (H) Western blot analysis showing the effects of UA (15, 20 or 25 µM) on the phosphorylation levels of AKT and mTOR in HCT15, HCT116, and MC38 cells, as well as the regulation of p-FOXO1, TCF1, GZMB, and p-AKT in hCD8⁺ T cells and CTLL-2 cells. P < 0.05 was considered statistically significant (* P < 0.05, ** P < 0.01, *** P < 0.001).
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    Urolithin A suppresses CRC cell proliferation and enhances T-cell activation. (A) Dose–response curves of UA in <t>HCT15,</t> HCT116, MC38, NCM460 and MCEC cells at 48 h and 72 h, with corresponding IC 50 values. The selectivity index (SI = IC 50 normal / IC 50 cancer) is shown for each cell line; (B-C) Effects of increasing concentrations of UA on the viability of CTLL-2 cells and human CD8 + T cells (hCD8 + T) at 48 h; (D) Schematic illustration of T-cell and tumor cell co-culture in the presence of UA; (E-G) Cell viability assays demonstrating that combined treatment with UA (20 or 25 µM) and T cells more effectively suppresses the proliferation of HCT15, HCT116, and MC38 cells compared with UA or T-cell treatment alone; (H) Western blot analysis showing the effects of UA (15, 20 or 25 µM) on the phosphorylation levels of AKT and mTOR in HCT15, HCT116, and MC38 cells, as well as the regulation of p-FOXO1, TCF1, GZMB, and p-AKT in hCD8⁺ T cells and CTLL-2 cells. P < 0.05 was considered statistically significant (* P < 0.05, ** P < 0.01, *** P < 0.001).
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    Correlation between the SNRPN , ZAC1, and INPP5F expression levels and methylation levels in <t>HCT15</t> cells. Increased expression levels of the three imprinted genes are accompanied by hypomethylation in HCT15 cells treated with 5‐Aza. Left: The SNRPN , ZAC1, and INPP5F methylation levels were compared between controls (cells treated with 0 μmol/μl 5‐Aza) and cells treated with 50 μmol/μL of 5‐Aza. The methylation levels of all the genes were decreased in 50‐μmol/μL 5‐Aza group. Right: The SNRPN , ZAC1, and INPP5F expression levels were compared between controls and cells treated with 50 μmol/μL of 5‐Aza. The expression levels of all the genes were increased in the 50‐μmol/μL 5‐Aza group. * P < .05, ** P < .01, *** P < .001
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    Urolithin A suppresses CRC cell proliferation and enhances T-cell activation. (A) Dose–response curves of UA in HCT15, HCT116, MC38, NCM460 and MCEC cells at 48 h and 72 h, with corresponding IC 50 values. The selectivity index (SI = IC 50 normal / IC 50 cancer) is shown for each cell line; (B-C) Effects of increasing concentrations of UA on the viability of CTLL-2 cells and human CD8 + T cells (hCD8 + T) at 48 h; (D) Schematic illustration of T-cell and tumor cell co-culture in the presence of UA; (E-G) Cell viability assays demonstrating that combined treatment with UA (20 or 25 µM) and T cells more effectively suppresses the proliferation of HCT15, HCT116, and MC38 cells compared with UA or T-cell treatment alone; (H) Western blot analysis showing the effects of UA (15, 20 or 25 µM) on the phosphorylation levels of AKT and mTOR in HCT15, HCT116, and MC38 cells, as well as the regulation of p-FOXO1, TCF1, GZMB, and p-AKT in hCD8⁺ T cells and CTLL-2 cells. P < 0.05 was considered statistically significant (* P < 0.05, ** P < 0.01, *** P < 0.001).

    Journal: Scientific Reports

    Article Title: Urolithin A blocks colorectal cancer progression by AKT1 inhibition–driven immune activation

    doi: 10.1038/s41598-026-45621-y

    Figure Lengend Snippet: Urolithin A suppresses CRC cell proliferation and enhances T-cell activation. (A) Dose–response curves of UA in HCT15, HCT116, MC38, NCM460 and MCEC cells at 48 h and 72 h, with corresponding IC 50 values. The selectivity index (SI = IC 50 normal / IC 50 cancer) is shown for each cell line; (B-C) Effects of increasing concentrations of UA on the viability of CTLL-2 cells and human CD8 + T cells (hCD8 + T) at 48 h; (D) Schematic illustration of T-cell and tumor cell co-culture in the presence of UA; (E-G) Cell viability assays demonstrating that combined treatment with UA (20 or 25 µM) and T cells more effectively suppresses the proliferation of HCT15, HCT116, and MC38 cells compared with UA or T-cell treatment alone; (H) Western blot analysis showing the effects of UA (15, 20 or 25 µM) on the phosphorylation levels of AKT and mTOR in HCT15, HCT116, and MC38 cells, as well as the regulation of p-FOXO1, TCF1, GZMB, and p-AKT in hCD8⁺ T cells and CTLL-2 cells. P < 0.05 was considered statistically significant (* P < 0.05, ** P < 0.01, *** P < 0.001).

    Article Snippet: Cell lines The colorectal cancer cell lines HCT15, HCT116, and MC38; the colonic epithelial cell line NCM460; and the human and murine lymphocyte cell lines CTLL-2 were obtained from Procell (Wuhan, China), while the murine colonic epithelial cell line MCEC was purchased from the ATCC cell bank.

    Techniques: Activation Assay, Co-Culture Assay, Western Blot, Phospho-proteomics

    Urolithin A suppresses CRC proliferation, migration, invasion, and enhances CD8⁺ T-cell infiltration. (A–B) Wound-healing assays and quantification showing that UA(20 μm) combined with lymphocytes (hCD8 + T cells or CTLL-2) markedly inhibits migration of HCT15, HCT116, and MC38 cells at 24 h and 48 h; (C–D) Transwell invasion and migration assays and quantification indicating that UA (20 μm) together with lymphocytes significantly reduces invasion index of HCT15, HCT116, and MC38 cells; (E)Schematic diagram of the MC38 orthotopic colorectal cancer mouse model and treatment regimen with UA (100 mg/kg/day); (F–G) Representative macroscopic images and tumor volume measurements demonstrating that UA treatment inhibits tumor growth; (H) Representative H&E staining of tumors from vehicle- and UA-treated mice; (I) Immunohistochemical staining of Ki67 showing decreased proliferation in UA-treated tumors; (J) Immunohistochemical staining of CD8 revealing enhanced CD8⁺ T-cell infiltration in UA-treated tumors; (K) Quantitative analysis showing that UA lowers the proliferation index and increases CD8⁺ T-cell infiltration in vivo . P < 0.05 was considered statistically significant (* P < 0.05, ** P < 0.01, *** P < 0.001).

    Journal: Scientific Reports

    Article Title: Urolithin A blocks colorectal cancer progression by AKT1 inhibition–driven immune activation

    doi: 10.1038/s41598-026-45621-y

    Figure Lengend Snippet: Urolithin A suppresses CRC proliferation, migration, invasion, and enhances CD8⁺ T-cell infiltration. (A–B) Wound-healing assays and quantification showing that UA(20 μm) combined with lymphocytes (hCD8 + T cells or CTLL-2) markedly inhibits migration of HCT15, HCT116, and MC38 cells at 24 h and 48 h; (C–D) Transwell invasion and migration assays and quantification indicating that UA (20 μm) together with lymphocytes significantly reduces invasion index of HCT15, HCT116, and MC38 cells; (E)Schematic diagram of the MC38 orthotopic colorectal cancer mouse model and treatment regimen with UA (100 mg/kg/day); (F–G) Representative macroscopic images and tumor volume measurements demonstrating that UA treatment inhibits tumor growth; (H) Representative H&E staining of tumors from vehicle- and UA-treated mice; (I) Immunohistochemical staining of Ki67 showing decreased proliferation in UA-treated tumors; (J) Immunohistochemical staining of CD8 revealing enhanced CD8⁺ T-cell infiltration in UA-treated tumors; (K) Quantitative analysis showing that UA lowers the proliferation index and increases CD8⁺ T-cell infiltration in vivo . P < 0.05 was considered statistically significant (* P < 0.05, ** P < 0.01, *** P < 0.001).

    Article Snippet: Cell lines The colorectal cancer cell lines HCT15, HCT116, and MC38; the colonic epithelial cell line NCM460; and the human and murine lymphocyte cell lines CTLL-2 were obtained from Procell (Wuhan, China), while the murine colonic epithelial cell line MCEC was purchased from the ATCC cell bank.

    Techniques: Migration, Staining, Immunohistochemical staining, In Vivo

    Correlation between the SNRPN , ZAC1, and INPP5F expression levels and methylation levels in HCT15 cells. Increased expression levels of the three imprinted genes are accompanied by hypomethylation in HCT15 cells treated with 5‐Aza. Left: The SNRPN , ZAC1, and INPP5F methylation levels were compared between controls (cells treated with 0 μmol/μl 5‐Aza) and cells treated with 50 μmol/μL of 5‐Aza. The methylation levels of all the genes were decreased in 50‐μmol/μL 5‐Aza group. Right: The SNRPN , ZAC1, and INPP5F expression levels were compared between controls and cells treated with 50 μmol/μL of 5‐Aza. The expression levels of all the genes were increased in the 50‐μmol/μL 5‐Aza group. * P < .05, ** P < .01, *** P < .001

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: Imprinting aberrations of SNRPN , ZAC1 and INPP5F genes involved in the pathogenesis of congenital heart disease with extracardiac malformations

    doi: 10.1111/jcmm.15584

    Figure Lengend Snippet: Correlation between the SNRPN , ZAC1, and INPP5F expression levels and methylation levels in HCT15 cells. Increased expression levels of the three imprinted genes are accompanied by hypomethylation in HCT15 cells treated with 5‐Aza. Left: The SNRPN , ZAC1, and INPP5F methylation levels were compared between controls (cells treated with 0 μmol/μl 5‐Aza) and cells treated with 50 μmol/μL of 5‐Aza. The methylation levels of all the genes were decreased in 50‐μmol/μL 5‐Aza group. Right: The SNRPN , ZAC1, and INPP5F expression levels were compared between controls and cells treated with 50 μmol/μL of 5‐Aza. The expression levels of all the genes were increased in the 50‐μmol/μL 5‐Aza group. * P < .05, ** P < .01, *** P < .001

    Article Snippet: The human colorectal cancer HCT15 cell line, which demonstrates global hypermethylation, was obtained from the American Type Culture Collection .

    Techniques: Expressing, Methylation