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ATCC human crc cell lines ht29
Effect of oleate treatment on cellular lipid accumulation in CRC cells. <t>HT29</t> and Caco‐2 cells were incubated with indicated oleate (OL) concentrations for 3–48 h. (A) Intracellular triglyceride levels were normalized to cellular protein content. (B) Representative light microscopic images of oil red O staining (400× magnification). (C) Free fatty acids in the supernatant of cells incubated with 0.4 mM OL at indicated time points. (D) PLIN2 mRNA expression analysed by quantitative RT‐PCR and protein expression analysed by western blot. (E) Representative images of immunofluorescence staining for PLIN2 (red) (Magn. 400×). Cell nuclei were stained with DAPI (blue) (* p < 0.05 compared to control (Ctr)).
Human Crc Cell Lines Ht29, 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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ATCC human crc cell lines sw1116
Effect of oleate treatment on cellular lipid accumulation in CRC cells. <t>HT29</t> and Caco‐2 cells were incubated with indicated oleate (OL) concentrations for 3–48 h. (A) Intracellular triglyceride levels were normalized to cellular protein content. (B) Representative light microscopic images of oil red O staining (400× magnification). (C) Free fatty acids in the supernatant of cells incubated with 0.4 mM OL at indicated time points. (D) PLIN2 mRNA expression analysed by quantitative RT‐PCR and protein expression analysed by western blot. (E) Representative images of immunofluorescence staining for PLIN2 (red) (Magn. 400×). Cell nuclei were stained with DAPI (blue) (* p < 0.05 compared to control (Ctr)).
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Classification of CRC cell lines by mismatch repair protein expression and cytotoxicity assessment of telmisartan. (A) Western blot analysis of MLH1, MSH2, MSH6, and PMS2 expression in CRC cell lines. <t>SW480</t> and CT26 showed intact expression of all four MMR proteins, indicating pMMR/MSS status. HCT116 showed loss of MLH1 and PMS2 expression, and HT29 showed loss of MSH6 expression, indicating dMMR/MSI-H status. (B) MMR protein expression in murine CT26 cells, showing intact expression (MSS). (C-E) Cell viability following telmisartan treatment (0–50 μM) for 24 hours in SW480 (C), HCT116 (D), and CT26 (E) cells as determined by CCK-8 assays. Data represent mean ± SD (n=5, three independent experiments). β-actin served as loading control. CCK-8, Cell Counting Kit-8; CRC, colorectal cancer; dMMR, deficient mismatch repair; DMSO, dimethyl sulfoxide; MMR, mismatch repair; MSI-H, high microsatellite instability; MSS, microsatellite stable; pMMR, proficient mismatch repair; SD, standard deviation.
Human Crc Cell Lines Sw480, 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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ATCC human crc cell lines
Classification of CRC cell lines by mismatch repair protein expression and cytotoxicity assessment of telmisartan. (A) Western blot analysis of MLH1, MSH2, MSH6, and PMS2 expression in CRC cell lines. <t>SW480</t> and CT26 showed intact expression of all four MMR proteins, indicating pMMR/MSS status. HCT116 showed loss of MLH1 and PMS2 expression, and HT29 showed loss of MSH6 expression, indicating dMMR/MSI-H status. (B) MMR protein expression in murine CT26 cells, showing intact expression (MSS). (C-E) Cell viability following telmisartan treatment (0–50 μM) for 24 hours in SW480 (C), HCT116 (D), and CT26 (E) cells as determined by CCK-8 assays. Data represent mean ± SD (n=5, three independent experiments). β-actin served as loading control. CCK-8, Cell Counting Kit-8; CRC, colorectal cancer; dMMR, deficient mismatch repair; DMSO, dimethyl sulfoxide; MMR, mismatch repair; MSI-H, high microsatellite instability; MSS, microsatellite stable; pMMR, proficient mismatch repair; SD, standard deviation.
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ATCC human crc derived cell lines
Classification of CRC cell lines by mismatch repair protein expression and cytotoxicity assessment of telmisartan. (A) Western blot analysis of MLH1, MSH2, MSH6, and PMS2 expression in CRC cell lines. <t>SW480</t> and CT26 showed intact expression of all four MMR proteins, indicating pMMR/MSS status. HCT116 showed loss of MLH1 and PMS2 expression, and HT29 showed loss of MSH6 expression, indicating dMMR/MSI-H status. (B) MMR protein expression in murine CT26 cells, showing intact expression (MSS). (C-E) Cell viability following telmisartan treatment (0–50 μM) for 24 hours in SW480 (C), HCT116 (D), and CT26 (E) cells as determined by CCK-8 assays. Data represent mean ± SD (n=5, three independent experiments). β-actin served as loading control. CCK-8, Cell Counting Kit-8; CRC, colorectal cancer; dMMR, deficient mismatch repair; DMSO, dimethyl sulfoxide; MMR, mismatch repair; MSI-H, high microsatellite instability; MSS, microsatellite stable; pMMR, proficient mismatch repair; SD, standard deviation.
Human Crc Derived 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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ATCC crc cell lines hct 116
Classification of CRC cell lines by mismatch repair protein expression and cytotoxicity assessment of telmisartan. (A) Western blot analysis of MLH1, MSH2, MSH6, and PMS2 expression in CRC cell lines. <t>SW480</t> and CT26 showed intact expression of all four MMR proteins, indicating pMMR/MSS status. HCT116 showed loss of MLH1 and PMS2 expression, and HT29 showed loss of MSH6 expression, indicating dMMR/MSI-H status. (B) MMR protein expression in murine CT26 cells, showing intact expression (MSS). (C-E) Cell viability following telmisartan treatment (0–50 μM) for 24 hours in SW480 (C), HCT116 (D), and CT26 (E) cells as determined by CCK-8 assays. Data represent mean ± SD (n=5, three independent experiments). β-actin served as loading control. CCK-8, Cell Counting Kit-8; CRC, colorectal cancer; dMMR, deficient mismatch repair; DMSO, dimethyl sulfoxide; MMR, mismatch repair; MSI-H, high microsatellite instability; MSS, microsatellite stable; pMMR, proficient mismatch repair; SD, standard deviation.
Crc Cell Lines Hct 116, 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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Effect of oleate treatment on cellular lipid accumulation in CRC cells. HT29 and Caco‐2 cells were incubated with indicated oleate (OL) concentrations for 3–48 h. (A) Intracellular triglyceride levels were normalized to cellular protein content. (B) Representative light microscopic images of oil red O staining (400× magnification). (C) Free fatty acids in the supernatant of cells incubated with 0.4 mM OL at indicated time points. (D) PLIN2 mRNA expression analysed by quantitative RT‐PCR and protein expression analysed by western blot. (E) Representative images of immunofluorescence staining for PLIN2 (red) (Magn. 400×). Cell nuclei were stained with DAPI (blue) (* p < 0.05 compared to control (Ctr)).

Journal: Journal of Cellular and Molecular Medicine

Article Title: Lipid Accumulation Promotes Tumorigenic Behaviour of Colorectal Cancer Cells

doi: 10.1111/jcmm.71393

Figure Lengend Snippet: Effect of oleate treatment on cellular lipid accumulation in CRC cells. HT29 and Caco‐2 cells were incubated with indicated oleate (OL) concentrations for 3–48 h. (A) Intracellular triglyceride levels were normalized to cellular protein content. (B) Representative light microscopic images of oil red O staining (400× magnification). (C) Free fatty acids in the supernatant of cells incubated with 0.4 mM OL at indicated time points. (D) PLIN2 mRNA expression analysed by quantitative RT‐PCR and protein expression analysed by western blot. (E) Representative images of immunofluorescence staining for PLIN2 (red) (Magn. 400×). Cell nuclei were stained with DAPI (blue) (* p < 0.05 compared to control (Ctr)).

Article Snippet: The human CRC cell lines HT29 (ATCC HTB‐38), Caco‐2 (ATCC HTB‐37), SW48 (ATCC CCL‐231), SW480 (ATCC CCL‐228), HCT116 (ATCC CCL‐247) and LoVo (ATCC CCL‐229) were cultured in DMEM supplemented with penicillin (400 U/mL), streptomycin (50 μg/mL), L‐glutamine (5840 mg/L), glucose (450 mg/dL) and 10% fetal calf serum (FCS) and incubated at 37°C in an 8% CO 2 atmosphere as described in [ ].

Techniques: Incubation, Staining, Expressing, Quantitative RT-PCR, Western Blot, Immunofluorescence, Control

Effect of lipid uptake on expression of key enzymes of lipid metabolism in CRC cells. HT29 and Caco‐2 cells were treated with indicated oleate (OL) concentrations for 12–24 h. (A) ACLY mRNA expression. (B) FASN mRNA expression. (C) SCD1 mRNA expression. (D) DGAT2 mRNA expression and (E) CPT1A mRNA expression analysed by quantitative RT‐PCR and CPT1A protein expression analysed by western blot. (F) ATGL protein expression analysed by western blot (* p < 0.05 compared to control (Ctr)).

Journal: Journal of Cellular and Molecular Medicine

Article Title: Lipid Accumulation Promotes Tumorigenic Behaviour of Colorectal Cancer Cells

doi: 10.1111/jcmm.71393

Figure Lengend Snippet: Effect of lipid uptake on expression of key enzymes of lipid metabolism in CRC cells. HT29 and Caco‐2 cells were treated with indicated oleate (OL) concentrations for 12–24 h. (A) ACLY mRNA expression. (B) FASN mRNA expression. (C) SCD1 mRNA expression. (D) DGAT2 mRNA expression and (E) CPT1A mRNA expression analysed by quantitative RT‐PCR and CPT1A protein expression analysed by western blot. (F) ATGL protein expression analysed by western blot (* p < 0.05 compared to control (Ctr)).

Article Snippet: The human CRC cell lines HT29 (ATCC HTB‐38), Caco‐2 (ATCC HTB‐37), SW48 (ATCC CCL‐231), SW480 (ATCC CCL‐228), HCT116 (ATCC CCL‐247) and LoVo (ATCC CCL‐229) were cultured in DMEM supplemented with penicillin (400 U/mL), streptomycin (50 μg/mL), L‐glutamine (5840 mg/L), glucose (450 mg/dL) and 10% fetal calf serum (FCS) and incubated at 37°C in an 8% CO 2 atmosphere as described in [ ].

Techniques: Expressing, Quantitative RT-PCR, Western Blot, Control

Effect of cellular lipid accumulation on tumorigenicity of cancer cells. HT29 and Caco‐2 cells were treated with indicated oleate (OL) concentrations for 12–24 h. (A) Proliferation and (B) migratory activity of CRC cells. mRNA expression of EMT‐markers (C) E‐CAD and N‐CAD and (D) SNAIL (E) and TWIST. (F) mRNA expression of IL‐8 (* p < 0.05 compared to control (Ctr)).

Journal: Journal of Cellular and Molecular Medicine

Article Title: Lipid Accumulation Promotes Tumorigenic Behaviour of Colorectal Cancer Cells

doi: 10.1111/jcmm.71393

Figure Lengend Snippet: Effect of cellular lipid accumulation on tumorigenicity of cancer cells. HT29 and Caco‐2 cells were treated with indicated oleate (OL) concentrations for 12–24 h. (A) Proliferation and (B) migratory activity of CRC cells. mRNA expression of EMT‐markers (C) E‐CAD and N‐CAD and (D) SNAIL (E) and TWIST. (F) mRNA expression of IL‐8 (* p < 0.05 compared to control (Ctr)).

Article Snippet: The human CRC cell lines HT29 (ATCC HTB‐38), Caco‐2 (ATCC HTB‐37), SW48 (ATCC CCL‐231), SW480 (ATCC CCL‐228), HCT116 (ATCC CCL‐247) and LoVo (ATCC CCL‐229) were cultured in DMEM supplemented with penicillin (400 U/mL), streptomycin (50 μg/mL), L‐glutamine (5840 mg/L), glucose (450 mg/dL) and 10% fetal calf serum (FCS) and incubated at 37°C in an 8% CO 2 atmosphere as described in [ ].

Techniques: Activity Assay, Expressing, Control

Classification of CRC cell lines by mismatch repair protein expression and cytotoxicity assessment of telmisartan. (A) Western blot analysis of MLH1, MSH2, MSH6, and PMS2 expression in CRC cell lines. SW480 and CT26 showed intact expression of all four MMR proteins, indicating pMMR/MSS status. HCT116 showed loss of MLH1 and PMS2 expression, and HT29 showed loss of MSH6 expression, indicating dMMR/MSI-H status. (B) MMR protein expression in murine CT26 cells, showing intact expression (MSS). (C-E) Cell viability following telmisartan treatment (0–50 μM) for 24 hours in SW480 (C), HCT116 (D), and CT26 (E) cells as determined by CCK-8 assays. Data represent mean ± SD (n=5, three independent experiments). β-actin served as loading control. CCK-8, Cell Counting Kit-8; CRC, colorectal cancer; dMMR, deficient mismatch repair; DMSO, dimethyl sulfoxide; MMR, mismatch repair; MSI-H, high microsatellite instability; MSS, microsatellite stable; pMMR, proficient mismatch repair; SD, standard deviation.

Journal: Translational Cancer Research

Article Title: Telmisartan enhances anti-PD-1 efficacy in MSS colorectal cancer via modulation of PD-L1 and STAT3 signaling

doi: 10.21037/tcr-2026-1409

Figure Lengend Snippet: Classification of CRC cell lines by mismatch repair protein expression and cytotoxicity assessment of telmisartan. (A) Western blot analysis of MLH1, MSH2, MSH6, and PMS2 expression in CRC cell lines. SW480 and CT26 showed intact expression of all four MMR proteins, indicating pMMR/MSS status. HCT116 showed loss of MLH1 and PMS2 expression, and HT29 showed loss of MSH6 expression, indicating dMMR/MSI-H status. (B) MMR protein expression in murine CT26 cells, showing intact expression (MSS). (C-E) Cell viability following telmisartan treatment (0–50 μM) for 24 hours in SW480 (C), HCT116 (D), and CT26 (E) cells as determined by CCK-8 assays. Data represent mean ± SD (n=5, three independent experiments). β-actin served as loading control. CCK-8, Cell Counting Kit-8; CRC, colorectal cancer; dMMR, deficient mismatch repair; DMSO, dimethyl sulfoxide; MMR, mismatch repair; MSI-H, high microsatellite instability; MSS, microsatellite stable; pMMR, proficient mismatch repair; SD, standard deviation.

Article Snippet: Human CRC cell lines SW480 (pMMR/MSS), HT29 (dMMR/MSI-H), and HCT116 (dMMR/MSI-H) were obtained from the American Type Culture Collection (ATCC).

Techniques: Expressing, Western Blot, Analysis, CCK-8 Assay, Control, Cell Counting, Standard Deviation

Telmisartan inhibits CRC cell migration and counteracts Ang II-induced effects. (A,B) Representative images (A) and quantification (B) of Transwell migration assays in SW480 (MSS) cells treated with vehicle control, telmisartan (10 or 20 μM), Ang II (100 nM), or combinations for 16 hours. (C,D) Representative images (C) and quantification (D) of migration assays in HCT116 (MSI-H) cells under identical conditions. Migrated cells were stained with crystal violet and counted in five random fields per membrane. Data represent mean ± SD from three independent experiments. Scale bar =100 μm. Ang, angiotensin; CRC, colorectal cancer; MSS, microsatellite stable; MSI-H, high microsatellite instability; SD, standard deviation.

Journal: Translational Cancer Research

Article Title: Telmisartan enhances anti-PD-1 efficacy in MSS colorectal cancer via modulation of PD-L1 and STAT3 signaling

doi: 10.21037/tcr-2026-1409

Figure Lengend Snippet: Telmisartan inhibits CRC cell migration and counteracts Ang II-induced effects. (A,B) Representative images (A) and quantification (B) of Transwell migration assays in SW480 (MSS) cells treated with vehicle control, telmisartan (10 or 20 μM), Ang II (100 nM), or combinations for 16 hours. (C,D) Representative images (C) and quantification (D) of migration assays in HCT116 (MSI-H) cells under identical conditions. Migrated cells were stained with crystal violet and counted in five random fields per membrane. Data represent mean ± SD from three independent experiments. Scale bar =100 μm. Ang, angiotensin; CRC, colorectal cancer; MSS, microsatellite stable; MSI-H, high microsatellite instability; SD, standard deviation.

Article Snippet: Human CRC cell lines SW480 (pMMR/MSS), HT29 (dMMR/MSI-H), and HCT116 (dMMR/MSI-H) were obtained from the American Type Culture Collection (ATCC).

Techniques: Migration, Control, Staining, Membrane, Standard Deviation

Telmisartan is associated with reduced PD-L1 expression and increased STAT3 phosphorylation. (A-C) Western blot analysis of PD-L1 protein expression in SW480 (MSS) (A), CT26 (MSS) (B), and HCT116 (MSI-H) (C) cells following treatment with telmisartan (0, 10, 20 μM) for 24 hours. (D) Western blot analysis of total STAT3 and phosphorylated STAT3 (p-STAT3, Tyr705) in SW480 cells treated with increasing concentrations of telmisartan (0–30 μM) for 24 hours. Densitometric quantification of p-STAT3/total STAT3 ratio is shown. β-actin served as loading control. Representative of three independent experiments. MSI-H, high microsatellite instability; MSS, microsatellite stable; PD-L1, programmed death-ligand 1; STAT3, signal transducer and activator of transcription 3.

Journal: Translational Cancer Research

Article Title: Telmisartan enhances anti-PD-1 efficacy in MSS colorectal cancer via modulation of PD-L1 and STAT3 signaling

doi: 10.21037/tcr-2026-1409

Figure Lengend Snippet: Telmisartan is associated with reduced PD-L1 expression and increased STAT3 phosphorylation. (A-C) Western blot analysis of PD-L1 protein expression in SW480 (MSS) (A), CT26 (MSS) (B), and HCT116 (MSI-H) (C) cells following treatment with telmisartan (0, 10, 20 μM) for 24 hours. (D) Western blot analysis of total STAT3 and phosphorylated STAT3 (p-STAT3, Tyr705) in SW480 cells treated with increasing concentrations of telmisartan (0–30 μM) for 24 hours. Densitometric quantification of p-STAT3/total STAT3 ratio is shown. β-actin served as loading control. Representative of three independent experiments. MSI-H, high microsatellite instability; MSS, microsatellite stable; PD-L1, programmed death-ligand 1; STAT3, signal transducer and activator of transcription 3.

Article Snippet: Human CRC cell lines SW480 (pMMR/MSS), HT29 (dMMR/MSI-H), and HCT116 (dMMR/MSI-H) were obtained from the American Type Culture Collection (ATCC).

Techniques: Expressing, Phospho-proteomics, Western Blot, Analysis, Control