Project description:miR-19b was up-regulated with hepatocellular carcinoma. We compared the transcriptional profile of Hep 3B transfected with miR-19b inhibitor with Hep3B transfected with control to identify genes affected by miR-19b knockdown. Hep 3B_miR-19b transfected vs Hep 3B_control transfected
Project description:This SuperSeries is composed of the following subset Series: GSE16340: Rat liver. Control vs. Chemical treated, 3 days GSE16394: Rat liver. Control vs. Chemical treated, 28 days GSE16743: Rat liver: Control vs. Chemical treated, 14 days Refer to individual Series
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 time-course (T0, 15, 30 min, 1, 3, 6 or 16 hours) of mRNA abundance changes was studied in the human Hep3B hepatoma cell line challenged with a pro-inflammatory cytokine-enriched medium (CM,conditionned medium) vs control medium (NCM,non conditionned medium). Paired cultures prepared from a same batch of trypsinized cells were challenged with CM vs NCM for a given length of time and this was repeated in three independent experiments (S1,S2,S3). Keywords: time-course
Project description:In this study, we investigated the biological roles and potential mechanisms of pentamethylquercetin (PMQ), a natural polymethyl flavones, against Hep3B liver cancer cells. Cell viability and growth curves were determined using the cell counting kit-8 (CCK-8) assay; flow cytometry was used to detect cell cycle and apoptosis; colony formation assay and JC-1 staining were used to detect cell proliferation and mitochondrial membrane potential changes, respectively. Transcriptome sequencing and western blotting were respectively used to investigate transcription and expression changes in Hep3B cells treated with PMQ. Treatment with 30 and 100 μM PMQ more significantly inhibited cell growth and proliferation in Hep3B cells than in HepG2 and LO2 cells. PMQ induced Hep3B cell cycle arrest and apoptosis by significantly reducing CDK4, CDK6, Cyclin D1, Cyclin E1, Cyclin B1 and Bcl-2 expression and increasing Bax, CDK1 and cleaved PARP levels. Transcriptomic profiles and western blotting results revealed that the MAPK and TNF signaling pathways may be involved in PMQ-induced Hep3B apoptosis.