Project description:Overexpression of SOX4 in various kinds of cancers specimen was associated with poor prognosis of patients; however, the role of SOX4 in angiogenesis or tumor microenvironment modulation remains unclear. Therefore the endogenous SOX4 was knockout and the differential gene expression between Hep3B and Hep3B SOX4-/- cells were examined via genechip. We found that the differentially expressed genes, EzH2, a SOX4-associated partner, and CXCL12, were repressed in Hep3B SOX4-/- cells compared with parental Hep3B; these results were further assessed via qRT-PCR in Hep3B SOX4-/- versus Hep3B cells.
Project description:We extracted the total RNA of Hep3B cells after silencing LINC01547 for 48 h and used RNA-seq technology to detect differentially expressed RNAs in Hep3B cells.
Project description:We extracted the total RNA of Hep3B cells treated with Bufotalin for 48 h and used RNA-seq technology to detect differentially expressed RNAs such as lncRNAs, miRNAs, and mRNAs in Hep3B cells.
Project description:A previous study from this laboratory demonstrated that up-regulating HNF4a could reverse the malignant phenotypes of HCC by inducing redifferentiation of HCC cells to hepatocytes. To study the mechanisms of the hepatic differentiation effect by HNF4α, we used the cDNA microarray to detect differential gene expression profiles of Hep3B infected with AdHNF4α and AdGFP. Expression profile analysis revealed that HNF4α positively regulated 1218 mRNAs and negatively regulated 1411 mRNAs for more than 2 times. The pathway analysis for the differential genes showed that the genes were involved in Complement and coagulation cascades, metabolism, Type II diabetes mellitus, Pathways in cancer etc.