Project description:Analysis of differentially expressed genes in colon cancer cell lines SW480 and HT29 with and without stably expressed ERbeta gene, with and without 10ng/mL TNFa treatment for 2 and 24 hours. Total RNA obtained from colon cancer cell lines SW480 and HT29 with and without stably expressed ERbeta gene, with and without 10ng/mL TNFa treatment for 2 and 24 hours.
Project description:Analysis of differentially expressed genes in colon cancer cell lines SW480 and HT29 with and without stably expressed ERbeta gene, with and without 10ng/mL TNFa treatment for 2 and 24 hours.
Project description:The WWOX gene is a tumor suppressor probably involved in regulation of cell cycle and apoptosis and downregulated in variety of cancer types.However, its role in colon cancerogenesis is unknown. The aim of this study was to characterize how WWOX may be involved in colon cancerogenesis or cancer progression, how it influences the basic cancer cell features and modifies cell expression profile.Our observations suggest that in HT29 colon cancer cell line increased expression of WWOX may result in transition of cancer cells into more normal- like colon epithelium phenotype, on the other hand in SW480 WWOX revealed the well-known tumour suppressor properties. However, as the colon cancer is very heterogeneous disease, obtained discrepancies may reflect the known differences between cell lines and cancerogenesis pathway, which they undergone. HT29 colon cancer cells were stably transfected with WWOX cDNA. HT29 cells transfected with an empty vector served as a control. Total mRNA was isolated to look for gene-expression differences induced by the WWOX overexpression.
Project description:The WWOX gene is a tumor suppressor probably involved in regulation of cell cycle and apoptosis and downregulated in variety of cancer types.However, its role in colon cancerogenesis is unknown. The aim of this study was to characterize how WWOX may be involved in colon cancerogenesis or cancer progression, how it influences the basic cancer cell features and modifies cell expression profile.Our observations suggest that in HT29 colon cancer cell line increased expression of WWOX may result in transition of cancer cells into more normal- like colon epithelium phenotype, on the other hand in SW480 WWOX revealed the well-known tumour suppressor properties. However, as the colon cancer is very heterogeneous disease, obtained discrepancies may reflect the known differences between cell lines and cancerogenesis pathway, which they undergone. SW480 colon cancer cells were stably transfected with WWOX cDNA. SW480 cells transfected with an empty vector served as a control. Total mRNA was isolated to look for gene-expression differences induced by the WWOX overexpression.
Project description:(Objectives) The goal of this study is to investigate paracrine effect of peripheral blood mononuclear cells (PBMCs) on colon cancer cell lines. (Method) Transcription profiles of PBMCs (control) and PBMCs co-cultured with colon cancer cell lines (treatment) were generated by deep sequencing, in triplicate for SW480 and duplicate for HT29, using Illumina HiSeq 4000. (Results and conclusion) Transcriptome analysis of PBMCs has shown the gene expression changed when co-cultured with colon cancer cell lines. The result revealed significantly up- and down-regulated genes.
Project description:By silencing of RALA, a downstream member of the RAS signal transduction pathway, we aimed to determine whether genes downstream of a mutated KRAS (codon 12 or 13) or a mutated BRAF can have significant functions in colorectal cancer carcinogenesis. RALA was silenced in three colorectal cancer cell lines (SW480, HCT116 and HT29). Effects were normalized to mock-transfected cells and the effects of scramble siRNA were excluded. SW480, HCT116 and HT29 cell lines were treated with the PI3K inhibitor LY294002 or DMSO.
Project description:Despite the growing recognition of the role of the stroma in cancer growth, invasive behavior and metastasis, the exact mechanisms of its participation remain unclear. We have explored the relationships between the epithelial/mesenchymal (E/M) state of colorectal cancer cells, their ability to activate fibroblasts, and the expression of collagen related genes. To this end, we studied (i) co-cultures of colorectal cancer cells with different hybrid E/M states and normal fibroblasts in a collagen matrix and (ii) patient-derived cancer-associated fibroblasts (CAFs). Using RNA-sequencing, we found that the different cancer cells can activate normal fibroblasts, which could form dense collagen networks. The functional enrichment analysis of differentially expressed genes indicates more mesenchymal phenotype and greater motility of SW480 cells compared to HT29 cells. The genes related to collagen biosynthesis and catabolism tend to be more active in SW480 cells rather than HT29 cells. Moreover, LOXL2 and LOXL3 genes, which are necessary for collagen fibril organization, are SW480 specific, which may indicate greater input of this cell line in collagen remodeling compared to HT29 cells. The expression of several CAF marker genes is activated in NFs upon co-cultivation with HT29 and SW480. Interestingly, a more-epithelial cell line HT29 activates the fibroblasts to a greater extent, than does SW480. The co-cultivation of colon cancer cell lines HT29 or SW480 with NFs leads to the activation of collagen biosynthesis and collagen fibril organization genes in NFs. Our findings suggest that the normal fibroblasts, activated by cancer cells, contribute to the organization of the extracellular matrix. Therefore, targeting the ability of cancer cells to activate normal fibroblasts can be considered as a new therapeutic strategy.
Project description:The WWOX gene is a tumor suppressor probably involved in regulation of cell cycle and apoptosis and downregulated in variety of cancer types.However, its role in colon cancerogenesis is unknown. The aim of this study was to characterize how WWOX may be involved in colon cancerogenesis or cancer progression, how it influences the basic cancer cell features and modifies cell expression profile.Our observations suggest that in HT29 colon cancer cell line increased expression of WWOX may result in transition of cancer cells into more normal- like colon epithelium phenotype, on the other hand in SW480 WWOX revealed the well-known tumour suppressor properties. However, as the colon cancer is very heterogeneous disease, obtained discrepancies may reflect the known differences between cell lines and cancerogenesis pathway, which they undergone.
Project description:The WWOX gene is a tumor suppressor probably involved in regulation of cell cycle and apoptosis and downregulated in variety of cancer types.However, its role in colon cancerogenesis is unknown. The aim of this study was to characterize how WWOX may be involved in colon cancerogenesis or cancer progression, how it influences the basic cancer cell features and modifies cell expression profile.Our observations suggest that in HT29 colon cancer cell line increased expression of WWOX may result in transition of cancer cells into more normal- like colon epithelium phenotype, on the other hand in SW480 WWOX revealed the well-known tumour suppressor properties. However, as the colon cancer is very heterogeneous disease, obtained discrepancies may reflect the known differences between cell lines and cancerogenesis pathway, which they undergone.
Project description:Purpose: To explore the effect of POLR1D on colorectal cancer cell lines HT29 and SW480. Methods: Whole transcriptome profiles of POLR1D knock down and AllStars Negative Control transfected colorectal cancer cell line (ie. HT29 and SW480) were generated by whole transcriptome sequencing, in replicate, using the Illumina NextSeq 550. The sequence reads that passed quality filters were analyzed at the gene level with Kallisto followed by DESeq2. Results: 45 genes showed consistent change after silencing of POLR1D, which included 2 genes that are well-known to be involved in the cell growth-related pathway, ie. VEGFA and EREG. Conclusions: POLR1D can infulence cell proliferation through VEGFA and EREG related pathway.