Project description:The TERT and HKR3 mechanism regulating cell cycle related expression changes remains unknown during HCC progress. We evaluated the relationship between hTERT expression and human kruppel-related 3 (HKR3) and cell cycle-related factors in Hep3B cell lines.
Project description:To evaluate small non-coding dysregulation in HCC cells, we sequenced hepatocellular carcinoma cell lines Huh7, HepG2, and Hep3B and normal liver cell HL7702 to compare their mall non-coding RNA profiles.
Project description:In order to explore the genetic changes of Hep3B cells after resistance to sorafenib, we used a dose-increasing method to obtain drug-resistant cell lines from parental Hep3B cells by intermittent stimulation with sorafenib.
Project description:The proteomic profiling of nine commonly used HCC cell lines Hep3B, HepG2, HepG2.2.15, HUH7, PLC/PRF/5, MHCC97L,MHCC97H,HCCLM3 and HCCLM6
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:Human hepatic cell lines have been widely used as an in vitro model for the study of drug metabolism and liver toxicity. However, the validity of this model is still a subject of debate because the expressions of various proteins including drug-metabolizing enzymes (DMEs) in the cell lines can differ significantly from that of human livers. In the present study, we first conducted an untargeted proteomics of the microsomes of the cell lines HepG2, Hep3B, and Huh7 in comparison with human livers using a SWATH method. Furthermore, a targeted proteomic approach, named high-resolution multiple reaction monitoring (MRM-HR), was utilized to compare the expressions of pre-selected DMEs between human livers and the cell lines.
Project description:Point mutations within the TERT promoter are the most common recurrent somatic non-coding mutation identified across different cancer types, including glioblastoma, melanoma, hepatocellular carcinoma and bladder cancer. They are most abundant at C146T and C124T and more rare at A57C, with the latter originally described as a familial case but subsequently shown also to occur somatically. All three mutations create de novo ETS (E-twenty-six specific) binding sites and result in the reactivation of the TERT gene, allowing cancer cells to achieve replicative immortality. Here, we employed a systematic proteomics screen to identify transcription factors preferentially binding to the C146T, C124T and A57C mutations. While we confirmed binding of multiple ETS factors to the mutant C146T and C124T sequences, we identified E4F1 a an A57C-specific binder and ZNF148 as a TERT WT binder that is excluded from the TERT promoter by the C124T allele. Both proteins are activating transcription factors that bind specifically to the A57C and wildtype (at position 124) TERT promoter sequence in corresponding cell lines and upregulate TERT transcription and telomerase activity.