Project description:CPT2 knockdown induced accumulation of glycerophospholipids and promoted CRC progression. We conducted transcriptomic sequencing of CPT2-knockdown HCT116 CRC cells to explore the underlying mechanism.
Project description:BORIS expresses abnormally in colorectal cancer cells. Both the expression and the copy number of BORIS are remarkably higher in colorectal cancer cells than in normal colon or rectal cells. BORIS is potential diagnosis, prognosis or therapeutic target for colorectal cancer. To expand our view of the signaling pathway related with BORIS, altered gene expression by BORIS knockdown was assessed by microarray assay. To study the gene regulation by BORIS knockdown, microarray assay was applied to screen the gene expression regulated by BORIS siRNA in colorectal cancer cells HCT116 and Caco-2
Project description:Epithelial-to-mesenchymal transition (EMT) is a fundamental process in development and disease. If aberrantly activated it is a trigger for tumour progression and metastasis (Thiery et al 2009 Cell). It is now known that EMT activation is also associated with the maintenance of stem-cell properties (Mani et al. 2008 Cell). Since Zinc-finger enhancer binding transcription factor 1 (ZEB1) is a crucial EMT activator, we analyzed the changes in the gene expression profile that accompany shRNA mediated loss of ZEB1 in HCT116 colorectal cancer cells. HCT116 is a cell line that exhibits mesenchymal characteristics, but reverts to an epithelial phenotype upon ZEB1 knock down (Spaderna et al. 2008 Cancer Research). HCT116 cells were stably transfected with control (GFP) or ZEB1 shRNA. Upon puromycin selection, single cell clones were picked and characterized. Cells from two control versus two ZEB1 knockdown clones were harvested, total RNA was isolated and processed to hybridization.
Project description:We sought to find out the molecular mechanism of CDK5 displayed in colorectal cancer. Microarray experiments were carried out to identify different gene expression between CDK5-knockdown HCT116 cell lines and Scramble HCT116 cell lines.
Project description:Transcriptional profiling of HCT116 cells transfected with either control siRNA or TET1 siRNA was analyzed using whole human genome microarrays. To identify genes regulated by TET1 in colorectal cancer, HCT116 cells were transfected with either control siRNA or TET1 siRNA, and total RNA was extracted from biologically duplicated samples.
Project description:We aimed to analyze the relationship between TET1 and aberrant CpG methylation in colorectal cancer (CRC). We established two stable TET1 knockdown clones and negative control clones of HCT116 cells, and carried out gene expression analysis with Agilent Human Gene Expression microarray kit.
Project description:We aimed to analyze the relationship between TET1 and aberrant CpG methylation in colorectal cancer (CRC). We established two stable TET1 knockdown clones and negative control clones of HCT116 cells, and carried out DNA methylation analysis with HumanMethylation450 BeadChip.
Project description:We have demonstrated that ELK4 promted progression and tumorigenesis in colorectal cancer. In order to elucidate the transcriptional regulation mechanism of ELK4 in colorectal cancer, RNA-seq analysis was performed on ELK4 knockdown and control HCT116 cells.
Project description:Sprouty proteins are evolutionarily conserved modulators of mitogen-activated protein kinase pathway. Sprouty2 appears to function as a tumor suppressor in cancers, whereas we reported earlier that Sprouty2 functions as an oncogene in colorectal cancer. To further understand the oncogenic potential of Sprouty2 in the colon, microRNA expression profile of colon cancer cells was investigated. Sprouty2 suppression in HCT116 colon cancer cells significantly increased MicroRNA 194-5p. Sprouty2 dependent regulation of microRNA194-5p and its biological targets were studied further for their tumor suppressive actions in reducing epithelial-mesenchymal transition in colorectal cancer. Sprouty2 knockdown was performed by infecting HCT116 cells with three different lentivirus expressing shRNAs against human Sprouty2 mRNA and a control non targeted non-silencing shRNA (Sprouty2 MISSION shRNA Lentiviral Transduction Particles; TRCN 0000007522, TRCN 0000231589, TRCN 0000231588 and a non-targeted shRNA control from Sigma) following lentiviral transduction protocols provided by Sigma. Due to the random integration of the lentivirus into the host genome, varying levels of Sprouty2 gene knockdown was expected in puromycin resistant colonies. Three colonies in triplicate that demonstrated highest to lowest level of Sprouty2 suppression, as assessed by western blotting, were selected. RNA samples from these colonies and one from non-targeted shRNA expressing colony were prepared for microRNA expression profile analysis. Pooled RNA samples from each group were shipped to Exiqon for microRNA profiling based on miRCURY LNATM array technology.
Project description:Determination of the ion channel and transporters gene expression profile of Bevacizumab-adapted colorectal adenocarcinoma cells HCT116