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: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.
Project description:SOX4 is a critical developmental transcription factor in vertebrates and is required for precise differentiation and proliferation in multiple tissues. In addition, SOX4 is overexpressed in many human malignancies, but the precise role of SOX4 in cancer progression is not well understood. Here we have either eliminated SOX4 using siRNA or overexpressed a SOX4 cDNA and compared the gene expression patterns against control GFP transfections to identify SOX4 target genes. Data described in manuscript P. Liu et al., Cancer Res 46, 4011 (April 15, 2006) Keywords: Gene Expression
Project description:To detect the gene profiles in decidualized stromal cells affected by SOX4, cultured stromal cells were transfected with siSOX4 and subjected to RNA-Seq. After aligned to mouse mm10 by HISAT2, RPKM value was calculated by Edger. Our results show that SOX4 was remarkable dimished after siSOX4 transfection. Meanwhile, some decidual marker genes were also changed significantly after SOX4 knockdow. The expression of SOX4 and other downstream genes were further confirmed by qPCR and westerblot. This RNA-Seq data provides fundamental information for our further physiological study of SOX4 during human stromal cells decidualization and fertility.
Project description:We knocked down SOX4 in T24 cell and created 3 cell lines: T24-scrambled, T24-SOX4-knockdown and T24-SOX4-rescue and compared gene expression changes SOX4 is a developmental transcription factor that is overexpressed in as many as 23% of bladder cancer patients, but the role of SOX4 in bladder cancer tumorigenesis is not well understood. Given SOX4’s many roles in embryonic development and context-dependent regulation of gene expression, we sought to understand SOX4’s contribution to bladder cancer and to elucidate SOX4 regulated genes that might contribute to tumorigenesis. We employed a CRISPR interference (CRISPRi) method to transcriptionally repress SOX4 expression in T24 bladder cancer cell lines, rescued these cell lines with lentivirally expressed SOX4, and performed whole genome expression profiling. SOX4 knockdown cells exhibited decreased invasive capabilities but no changes in migration or proliferation, while rescue with SOX4 lentiviral vector restored the invasive phenotype. Gene expression profiling revealed 173 high confidence SOX4 regulated genes
Project description:This SuperSeries is composed of the following subset Series: GSE11874: Chromatin Immunoprecipitation microarray data from antiHA IP in stable LNCaP cells expressing either YFP or HA-SOX4/YFP GSE11913: Illumina expression data from LNCaP cells overexpressing either SOX4 or GFP GSE11914: Expression data from LNCaP cells transfected with SOX4 cDNA, SOX4 siRNA or GFP cDNA Refer to individual Series
Project description:Sox4 is upregulated in adenoid cystic carcinoma (ACC). The ACC3 cell line is the most widely available cell culture model system of this tumor type. RNAi mediated knockdown of Sox4 in ACC3 cells induces apoptosis. Since Sox4 is a transcription factor, it is hypothesized that this apoptotic phenotype is due to changes in transcription from genes under Sox4 control.This experiment was designed to find candidate genes whose expression levels change after Sox4 knockdown that could contribute to the pro-apoptotic phenotype. Keywords: gene knockdown