cell line hct15  (Procell Inc)

Journal: Frontiers in Immunology

Article Title: Unveiling tumor senescence-driven prognostic heterogeneity via MALISS in stage II/III colorectal cancer

doi: 10.3389/fimmu.2025.1744719

Figure Lengend Snippet: NR1D2 promotes the CRC migration. (A) The importance of 30 immunosenescence-related genes selected by Coxboost algorithm. (B) Kaplan-Meier survival curve of PFS between patients with high NR1D2 and low NR1D2 mRNA level. (C) The NR1D2 expression of mRNA and protein levels within native control, siNR1D2#1, siNR1D2#2 and siNR1D2#3. Relative band intensity (normalized) is shown below the WB image. (D) SA-β-gal staining to analyze the senescence status in the HCT15 cells within native control, siNR1D2#1, siNR1D2#2 and siNR1D2#3. (E) P16 and P21 protein levels assessed by Western blot after NR1D2 knocking down. (F) Changes in mRNA expression of SASP-associated secretory factors (TGF-β, GDF15) as determined by qRT-PCR. (G) Wound healing assays was performed to detect the migration within native control, siNR1D2#1, siNR1D2#2 and siNR1D2#3 in HCT15. (H) Transwell assays was performed to detect the migration within native control, siNR1D2#1, siNR1D2#2 and siNR1D2#3 in HCT15. * means P < 0.05, ** means P < 0.01, *** means P < 0.001, **** means P < 0.0001.

Article Snippet: The HCT15 cell line (RRID: CVCL_0292), which was cultured in RPMI-1640 (Gibco) medium with 10% fetal bovine serum (Vazyme), penicillin-streptomycin (100 U/mL, NCM), was procured from ATCC.

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

Journal: Cancer & Metabolism

Article Title: NSUN2 promotes colorectal cancer progression by stabilizing PHGDH mRNA to promote serine metabolism reprogramming

doi: 10.1186/s40170-025-00406-1

Figure Lengend Snippet: NSUN2 enhances the tumorigenesis and progression of CRC. A , B) After infection of SW620 (A) and HCT116 (B) cells with shRNAs, the expression of NSUN2 was analsyzed by Western blot (left) and qRT-PCR (right) assays. C) After infection of HCT15 cells with NSUN2-WT plasmids, the expression of NSUN2 was analyzed by Western blot (left) and qRT-PCR (right) assays. D-E) After knocking down NSUN2 in SW620 (D) and HCT116 (E) cells, cell proliferation ability was measured by the CCK8 assay. F) After knocking down NSUN2 in SW620 and HCT116 cells, cell colony formation ability was measured by the colony formation experiments. G) Cell proliferation ability was assessed using the CCK8 assay following NSUN2 overexpression in HCT15 cells. H) After overexpressing NSUN2 in HCT15 cells, cell proliferation ability was assessed by colony formation assay. I-J) After knocking down NSUN2 in SW620 (I) and HCT116 (J) cells, cell migration and invasion were determined by transwell assays. scale bars = 100 μm. K) After overexpressing NSUN2 in HCT115 cells, cell migration and invasion were determined by transwell assays. scale bars = 100 μm

Article Snippet: The human CRC cell lines HCT15, HCT116, SW620 were purchased from the American Type Culture Collection (ATCC).

Techniques: Infection, Expressing, Western Blot, Quantitative RT-PCR, CCK-8 Assay, Over Expression, Colony Assay, Migration

Journal: Cancer & Metabolism

Article Title: NSUN2 promotes colorectal cancer progression by stabilizing PHGDH mRNA to promote serine metabolism reprogramming

doi: 10.1186/s40170-025-00406-1

Figure Lengend Snippet: NSUN2 promotes PHGDH expression in CRC. (A) Venn diagram of RNA-seq in NSUN2-stably knockdown HCT15 cells and combined it with MeRIP-seq data from the GEO public database ( GSE226129 ) to evaluate potential targets. Differential gene analysis between samples was carried out and screened by fold-change and P value. (B) PHGDH, PLEKHG2, VGF, LAMA5, KCTD15 and C6orf141 mRNA expression in SW620 cells and HCT116 cells with NSUN2 knockdown were detected by qRT-PCR. (C) Analyzing protein expression levels of PHGDH in SW620 and HCT116 cells after infection with shNSUN2-1 and shNSUN2-2. (D) Analyzing mRNA expression levels of PHGDH in SW620 and HCT116 cells after infection with shNSUN2-1 and shNSUN2-2. E , F) PHGDH was highly expressed in tumor tissues compared with adjacent normal tissues from GSE21510 (E) and TCGA (F) databases. G) Representative IHC staining images for PHGDH protein in human CRC specimens (scale bars = 250 μm and 50 μm), demonstrating its differential expression between tumor ( n = 56) and adjacent normal ( n = 56) tissue. H) Kaplan-Meier analysis of OS in the Renji Hospital cohort ( n = 180), comparing CRC patients with high ( n = 96) versus low ( n = 84) tumor PHGDH expression. I) NSUN2 were positively correlated with the expression of PHGDH at mRNA levels in TCGA databases. J) Tumor tissues and normal tissues from CRC patients were collected, and Western blot was used to analyze the levels of the NSUN2 and PHGDH proteins. K) Representative IHC staining for NSUN2 and PHGDH from CRC tissue (scale bars = 250 μm and 50 μm). Tumor 1# is representative of a patient with NSUN2-low CRC. Tumor 2# is representative of a patient with NSUN2-high CRC. L) Correlation of NSUN2 and PHGDH staining in human CRC tissue samples ( n = 180). NSUN2 and PHGDH show a positive correlation. ns, non-significant

Article Snippet: The human CRC cell lines HCT15, HCT116, SW620 were purchased from the American Type Culture Collection (ATCC).

Techniques: Expressing, RNA Sequencing, Stable Transfection, Knockdown, Quantitative RT-PCR, Infection, Immunohistochemistry, Quantitative Proteomics, Western Blot, Staining

Journal: The Turkish Journal of Gastroenterology

Article Title: m6A Methylation Regulator RBM15-Mediated Upregulation of ITGBL1 mRNA Stability Aggravates Colon Adenocarcinoma Progression by Remodeling the Tumor Microenvironment

doi: 10.5152/tjg.2025.24068

Figure Lengend Snippet: Expression pattern of ITGBL1 in COAD. (A) The TIMER database was used to display the differential expression of ITGBL1 in the Cancer Genome Atlas (TCGA) pan-cancer dataset. (B) UALCAN database showed ITGBL1 expression in COAD based on sample types TCGA samples. (C and E) The UALCAN database shows the association between ITGBL1 expression and COAD individual cancer stage, nodal metastatic status, and histologic subtype. (F and G) KM plotter database was used to analyze the relationship between ITGBL1 expression and RFS and OS of COAD. (H) Immunohistochemical observation of ITGBL1 expression in normal and COAD tissues. (I) RT-qPCR assay was used to detect the expression level of ITGBL1 in 45 normal tissues and 46 COAD tumor tissues. (J and K) Western blot analysis of ITGBL1 protein level in normal tissues, COAD tumor tissues, NCM460 cell line, and COAD cell lines (DLD1, Lovo, HCT15, and SW620). ** P < .01, *** P < .001.

Article Snippet: Colon adenocarcinoma cell lines (DLD1, CL-0074; HCT15, CL-0097; Procell, Wuhan, China) were cultivated in corresponding media (CM-0074, CM-0097, Procell) at 37°C with 5% CO 2 .

Techniques: Expressing, Quantitative Proteomics, Immunohistochemical staining, Quantitative RT-PCR, Western Blot

Journal: The Turkish Journal of Gastroenterology

Article Title: m6A Methylation Regulator RBM15-Mediated Upregulation of ITGBL1 mRNA Stability Aggravates Colon Adenocarcinoma Progression by Remodeling the Tumor Microenvironment

doi: 10.5152/tjg.2025.24068

Figure Lengend Snippet: Effects of ITGBL1 downregulation in COAD cell proliferation, migration, invasion, and EMT. Lovo and SW620 cells were transfected with sh-NC, sh-ITGBL1#1, or sh-ITGBL1#2. (A) ITGBL1 protein level was determined using western blot in transfected Lovo and SW620 cells. (B and C) Cell viability and proliferation were measured in transfected Lovo and SW620 cells using CCK-8 and colony formation assays. (D and E) Cell migration and invasion were assessed using Transwell assays in transfected Lovo and SW620 cells. (F) Western blot analysis of E-cadherin, Vimentin, and N-cadherin protein levels in transfected Lovo and SW620 cells. *** P < .01.

Article Snippet: Colon adenocarcinoma cell lines (DLD1, CL-0074; HCT15, CL-0097; Procell, Wuhan, China) were cultivated in corresponding media (CM-0074, CM-0097, Procell) at 37°C with 5% CO 2 .

Techniques: Migration, Transfection, Western Blot, CCK-8 Assay

Journal: The Turkish Journal of Gastroenterology

Article Title: m6A Methylation Regulator RBM15-Mediated Upregulation of ITGBL1 mRNA Stability Aggravates Colon Adenocarcinoma Progression by Remodeling the Tumor Microenvironment

doi: 10.5152/tjg.2025.24068

Figure Lengend Snippet: Inhibiting ITGBL1 impaired COAD cell growthin vivo. SW620 cells stably infected with sh-NC or sh-ITGBL1 were respectively subcutaneously inoculated into mice. (A and B) Tumor growth curve of xenografts and representative images of the tumors at the end of the experiment were presented. (C) Tumor weight was measured. (D) IHC staining was performed to measure the positive expression of ITGBL1, Ki-67, N-cadherin, E-cadherin, and Vimentin in xenografts. ** P < .01, *** P < .001.

Article Snippet: Colon adenocarcinoma cell lines (DLD1, CL-0074; HCT15, CL-0097; Procell, Wuhan, China) were cultivated in corresponding media (CM-0074, CM-0097, Procell) at 37°C with 5% CO 2 .

Techniques: Stable Transfection, Infection, Immunohistochemistry, Expressing

Journal: The Turkish Journal of Gastroenterology

Article Title: m6A Methylation Regulator RBM15-Mediated Upregulation of ITGBL1 mRNA Stability Aggravates Colon Adenocarcinoma Progression by Remodeling the Tumor Microenvironment

doi: 10.5152/tjg.2025.24068

Figure Lengend Snippet: ITGBL1 regulates the immune response to cancer. (A) TIMER database displayed the correlation of ITGBL1 with tumor-infiltrating immune cells (CD8 + T cells, macrophages, CD4 + T cells, B cells, neutrophils, and myeloid dendritic cells) in COAD. (B) GEPIA database exhibited correlation of ITGBL1 with tumor-associated M2-type macrophage markers (MRC1, CD163, IL-10, and TGFB1) and PD-L1 (CD274) expression in COAD. (C) Expression association between ITGBL1 and PD-L1 in COAD tissues was evaluated using Pearson correlation analysis. (D-G) Lovo and SW620 cells were transfected with sh-NC or sh-ITGBL1. Then, CM of transfected Lovo and SW620 cells were co-culture with isolated macrophages (THP1-M0). (D) The proportion of CD206 + positive cells was measured using flow cytometry. (E and F) CD163, CD206, and IL-10 mRNA levels were detected using RT-qPCR. (G) CD163, CD206, and IL-10 protein levels were assessed using a western blot assay. (H and I) Effector CD8 + T cells were co-cultured with indicated target Lovo and SW620 cells. (H) CD8 + T cell proliferation was examined using CFSE staining. (I) CD8 + T cell apoptosis was monitored by flow cytometry assay. ** P < .01, *** P < .001.

Article Snippet: Colon adenocarcinoma cell lines (DLD1, CL-0074; HCT15, CL-0097; Procell, Wuhan, China) were cultivated in corresponding media (CM-0074, CM-0097, Procell) at 37°C with 5% CO 2 .

Techniques: Expressing, Transfection, Co-Culture Assay, Isolation, Flow Cytometry, Quantitative RT-PCR, Western Blot, Cell Culture, Staining

Journal: The Turkish Journal of Gastroenterology

Article Title: m6A Methylation Regulator RBM15-Mediated Upregulation of ITGBL1 mRNA Stability Aggravates Colon Adenocarcinoma Progression by Remodeling the Tumor Microenvironment

doi: 10.5152/tjg.2025.24068

Figure Lengend Snippet: RBM15 stabilizes ITGBL1 expression through methylation modification. (A) Changes in the m6A methylation level of ITGBL1 after inhibition of RBM15 were analyzed by MeRIP-qPCR assay. (B) Their interaction was verified using a dual-luciferase reporter assay in Lovo and SW620 cells. (C) ITGBL1 mRNA level was measured in Lovo and SW620 cells transfected with sh-NC, sh-RBM15, vector, or RBM15 using RT-qPCR. (D) RBM15 and ITGBL1 protein levels were assessed in Lovo and SW620 cells transfected with sh-NC, sh-RBM15, vector, or RBM15 using western blot. (E-H) The UALCAN database exhibited the association between RBM15 expression and COAD sample types, individual cancer stages, nodal metastatic status, and histologic subtypes. (I) The KM plotter database was applied to analyze the relationship between RBM15 expression and the OS of COAD. (J) IHC staining was used to detect the positive expression of RBM15 in normal and COAD tissues. (K) RBM15 mRNA level was determined in 45 normal tissues and 46 COAD tumor tissues using RT-qPCR. (L and M) Western blot analysis of RBM15 protein levels in normal tissues, COAD tumor tissues, NCM460 cell line, and COAD cell lines (Lovo and SW620). ** P < .01, *** P < .001.

Article Snippet: Colon adenocarcinoma cell lines (DLD1, CL-0074; HCT15, CL-0097; Procell, Wuhan, China) were cultivated in corresponding media (CM-0074, CM-0097, Procell) at 37°C with 5% CO 2 .

Techniques: Expressing, Methylation, Modification, Inhibition, Luciferase, Reporter Assay, Transfection, Plasmid Preparation, Quantitative RT-PCR, Western Blot, Immunohistochemistry

Journal: The Turkish Journal of Gastroenterology

Article Title: m6A Methylation Regulator RBM15-Mediated Upregulation of ITGBL1 mRNA Stability Aggravates Colon Adenocarcinoma Progression by Remodeling the Tumor Microenvironment

doi: 10.5152/tjg.2025.24068

Figure Lengend Snippet: RBM15/ITGBL1 regulated COAD cell proliferation, migration, invasion, and EMT. (A) The transfection efficiency of sh-RBM15#1 or sh-RBM15#2 in Lovo and SW620 cells was measured using western blot. (B-G) Lovo and SW620 cells were transfected with sh-NC, sh-RBM15#1, sh-RBM15#1+ vector, or sh-RBM15#1+ITGBL1. (B) Western blot analysis of RBM15 protein levels in transfected Lovo and SW620 cells. (C and D) CCK-8 and colony formation assays were performed to assess cell viability and proliferation. (E and F) Transwell assays were conducted to measure cell migration and invasion. (G) E-cadherin, Vimentin, and N-cadherin protein levels were determined using western blot. ** P < .01, *** P < .001.

Article Snippet: Colon adenocarcinoma cell lines (DLD1, CL-0074; HCT15, CL-0097; Procell, Wuhan, China) were cultivated in corresponding media (CM-0074, CM-0097, Procell) at 37°C with 5% CO 2 .

Techniques: Migration, Transfection, Western Blot, Plasmid Preparation, CCK-8 Assay

Journal: The Turkish Journal of Gastroenterology

Article Title: m6A Methylation Regulator RBM15-Mediated Upregulation of ITGBL1 mRNA Stability Aggravates Colon Adenocarcinoma Progression by Remodeling the Tumor Microenvironment

doi: 10.5152/tjg.2025.24068

Figure Lengend Snippet: m6A methylase RBM15-mediated upregulation of ITGBL1 mRNA stability could boost COAD cell proliferation, migration, invasion, EMT, and immune escape.

Article Snippet: Colon adenocarcinoma cell lines (DLD1, CL-0074; HCT15, CL-0097; Procell, Wuhan, China) were cultivated in corresponding media (CM-0074, CM-0097, Procell) at 37°C with 5% CO 2 .

Techniques: Migration

Journal: bioRxiv

Article Title: Metabolic modulation of intratumoral cholesterol with gut microbiota for the treatment of colorectal cancer

doi: 10.1101/2025.05.02.651972

Figure Lengend Snippet: (a-e) Levels of cholesterol and its microbial metabolites 5-cholesten-3-one (5-C-3), 4-cholesten-3-one (4-C- 3), coprostanone, and coprostanol in CRC tumor biopsies and in adjacent normal tissues. (mean ± s.e.m. n=12; Unpaired t test). (f-g) Fecal cholesterol and 4-C-3 levels in a CRC patient cohort with 532 samples. (mean ± s.e.m ; Unpaired t test). (h-n) MTT assay in a panel of human colorectal cancer cell lines (HCT15, HT55, colo205, HCT116, DLD-1, Caco2 and YMAC) treated with indicated microbial metabolites of cholesterol for 48 h. (mean ± s.e.m., n=3). (o-p) Flow cytometry analyses of cell apoptosis in DLD1 and HCT116 cells treated with indicated microbial metabolites of cholesterol for 48 h. The quantification of apoptotic rates is shown in (p) . (mean ± s.e.m. n=3; one-way ANOVA). (q) Cell viability of colorectal cancer organoids derived from two patients with CRC upon the treatment with 4-C-3 at indicated dosages. (mean ± s.e.m., n=3; one-way ANOVA).

Article Snippet: HCT116, Caco-2, SW620, HT55, HT29, Colo205, YAMC, DLD-1, LS513, MC38, and HCT15 cell lines were purchased from ATCC (Manassas, VA, USA).

Techniques: MTT Assay, Flow Cytometry, Derivative Assay

Journal: Oncotarget

Article Title: Statins exhibit anti-tumor potential by modulating Wnt/β-catenin signaling in colorectal cancer

doi: 10.18632/oncotarget.28755

Figure Lengend Snippet: ( A ) Downregulated proteins represented in GO term (plotted on g:Profiler) upon statin treatment of HCT15 cells. ( B ) Immunoblot analysis of the effect of simvastatin treatment on select Wnt target proteins revealed their downregulation. ( C ) Log-fold change was observed in the peptide counts of YAP, β-catenin, and Cullin-3 in control versus statin-treated proteomics analysis, whereas no alteration was observed in housekeeping proteins like GAPDH and actin. Biological replicates = 3, with statistical significance of ** p < 0.005, **** p < 0.00005, ns is non-significant according to Students’ t -test analysis. ( D ) Immunoblots depicting SATB1 and SATB2 protein levels in HCT15 cells upon simvastatin treatment. SATB1 protein was significantly reduced, whereas SATB2 expression slightly increased upon simvastatin treatment.

Article Snippet: HCT116 and HCT15 CRC cell lines were obtained from the European Collection of Cell Cultures (ECACC) and HT29 cell line was obtained from American Type Culture Collection (ATCC, Manassas, VA, USA).

Techniques: Western Blot, Control, Expressing

Journal: Oncotarget

Article Title: Statins exhibit anti-tumor potential by modulating Wnt/β-catenin signaling in colorectal cancer

doi: 10.18632/oncotarget.28755

Figure Lengend Snippet: ( A ) Immunoblots depicting protein level alterations in β-catenin, SATB1 and SATB2 upon simvastatin treatment and mevalonate supplementation in HCT15 cells. Mevalonate supplementation resulted in the rescue of the protein levels of β-catenin and SATB1. ( B ) Relative transcript expression of β-catenin, SATB1 and SATB2 upon simvastatin treatment and mevalonate supplementation. No significant changes were observed in the transcript levels of any of these genes. ( C ) Relative levels of cholesterol upon mevalonate supplementation and simvastatin treatment in HCT-15 cells monitored by LC-MS analysis. Cholesterol level was reduced upon treatment with simvastatin or mevalonate and restored upon combined treatment with simvastatin plus mevalonate as compared to the untreated control. Biological replicates n = 3, ** p < 0.05, *** p < 0.005, ns is non-significant as per Students’ t -test analysis. ( D ) A model illustrating the impact of these two conditions on the feedback mechanism regulating cholesterol-responsive genes. The decreased cholesterol levels observed with mevalonate supplementation could be attributed to the feedback system, which suppresses cholesterol-responsive gene expression in the presence of excess mevalonate.

Article Snippet: HCT116 and HCT15 CRC cell lines were obtained from the European Collection of Cell Cultures (ECACC) and HT29 cell line was obtained from American Type Culture Collection (ATCC, Manassas, VA, USA).

Techniques: Western Blot, Expressing, Liquid Chromatography with Mass Spectroscopy, Control, Gene Expression

Journal: Oncotarget

Article Title: Statins exhibit anti-tumor potential by modulating Wnt/β-catenin signaling in colorectal cancer

doi: 10.18632/oncotarget.28755

Figure Lengend Snippet: ( A ) Images of spheroids for CRC cell lines HCT15, HCT116, HT29 which were grown in matrigel for 4 days. The panels depict phase contrast images of spheroids, scale bar 50 μm, zoomed in images in adjacent boxes. ( B ) Relative gene expression of SATB1, SATB2, β-catenin and EMT-MET markers, Vimentin and E-cadherin, respectively. The spheroids exhibited a higher expression of EMT marker Vimentin along with a higher expression of SATB1 than SATB2. β-catenin levels were unaltered. ( C ) Immunoblot to validate the protein levels of the EMT marker Vimentin and MET marker E-cadherin in 2D grown HCT15 cells versus the 3D spheroids of HCT15 cells. Vimentin protein is significantly upregulated in 3D spheroids. ( D ) Immunoblot to observe the protein levels of SATB1 and 2 in 2D and 3D spheroids of HCT15 cells recapitulating the tumorigenic phenotype of spheroids. ( E ) Colony formation assay using HCT15 cells upon simvastatin treatment and ( F ) graph representing no. of colonies in control versus treated sets. The colonies were allowed to form on soft agar for 5 days and thereafter treated with simvastatin for additional 48 h. The number of colonies were significantly reduced upon simvastatin treatment. Biological replicates n = 3, * p < 0.05, ** p < 0.005 as per Students’ t -test analysis.

Article Snippet: HCT116 and HCT15 CRC cell lines were obtained from the European Collection of Cell Cultures (ECACC) and HT29 cell line was obtained from American Type Culture Collection (ATCC, Manassas, VA, USA).

Techniques: Gene Expression, Expressing, Marker, Western Blot, Colony Assay, Control

Journal: Oncotarget

Article Title: Statins exhibit anti-tumor potential by modulating Wnt/β-catenin signaling in colorectal cancer

doi: 10.18632/oncotarget.28755

Figure Lengend Snippet: ( A ) Images depicting the effect of simvastatin on HT29 and HCT15 spheroids, wherein the treated set depicts disintegration of the spheroids. The images are captured using a phase contrast microscope, scale bar 400 μm (orange). The manually zoomed-in image in the adjacent square box clearly depicts a disintegrated spheroid morphology upon simvastatin treatment. The spheroids were generated over 4 days, thereafter, treated with simvastatin for additional 48 h. ( B ) Relative expression at transcript levels of SATB1, SATB2, β-catenin in spheroids with and without simvastatin treatment recapitulate the results from 2D cell lines of no alteration at transcript level. However, the E-cadherin transcript levels were significantly upregulated upon simvastatin treatment, suggesting transition to an epithelial phenotype. ( C ) Immunoblot to validate the protein expression of EMT marker vimentin and MET marker E-cadherin in untreated and statin treated spheroids respectively. The vimentin protein levels are significantly reduced upon simvastatin treatment. ( D ) Immunofluorescence assay in the 3D spheroids to determine the expression profile of Vimentin and E-cadherin upon statin treatment. The treated spheroids exhibit a disintegrated morphology with significant reduction in vimentin intensity, whereas, E-cadherin remains unaltered, corroborating with the results from immunoblot analysis. Scale bar 50 μm ( E ) Immunoblot to monitor the protein levels of SATB1 and SATB2 in statin-treated spheroids. The densitometry graph below depict the normalized intensities of SATB1 and SATB2. SATB1 levels were significantly reduced, whereas SATB2 levels were not significantly altered upon simvastatin treatment. ( F ) Immunofluorescence assay in the 3D spheroids to determine the expression profile of SATB1 upon simvastatin treatment which is significantly reduced in treated spheroids. The 3D reconstruction panel on the right shows an overall reduction in intensity. Scale bar 50 μm. ( G ) Immunofluorescence assay in the 3D spheroids to determine the expression profile of SATB2 in spheroids. The intensity of SATB2 staining is not altered upon simvastatin treatment, corroborating with the results from immunoblots. The 3D reconstruction of spheroids also depicts a holistic expression of unaltered SATB2 levels. Scale bar 20 μm. Biological replicates n = 4, * p < 0.05, ns is non-significant as per Student’s t -test analysis.

Article Snippet: HCT116 and HCT15 CRC cell lines were obtained from the European Collection of Cell Cultures (ECACC) and HT29 cell line was obtained from American Type Culture Collection (ATCC, Manassas, VA, USA).

Techniques: Microscopy, Generated, Expressing, Western Blot, Marker, Immunofluorescence, Staining