HBV VIS Detail Information

> This page shows VIS [1019992] detail information, including site information (chromosome, GRCh38 location, disease, sample, etc) and literature information.


Site Information
DVID 1019992
Chromosome chr20
GRCh38 Location 64303861
Disease Carcinoma, Hepatocellular  
Sample Cell line
Virus Reference Genome HE815465.1
Target Gene LINC00266-1  
Literature Information
PubMed PMID 31417659
Year 2019 Jul 10;10(17):4142-4150
Journal Journal of Cancer
Title HBV Integration-mediated Cell Apoptosis in HepG2.2.15.
Author Hu X,Jiang J,Ni C,Xu Q,Ye S,Wu J,Ge F,Han Y,Mo Y,Huang D,Yang L
Evidence Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer and the second leading cause of cancer deaths in the word. Hepatitis B virus (HBV) infection plays an important role in the development of HCC. However, the mechanisms by which HBV integration affects host cells remain poorly understood. HepG2.2.15 cell line is derived from HCC cell line HepG2 with stable transfection HBV expression. In this study, HepG2.2.15 cells showed decreased proliferation, G1 cell cycle arrest and increased apoptosis, when compared to HepG2 cells. HBV capture sequencing was conducted in both genome and transcriptome level, followed by RNA expression sequencing in HepG2.2.15. Here, CAMSAP2/CCDC12/DPP7/OR4F3 were found to be targets for HBV integration in both genome and transcriptome level, accompanied by alteration in their expression when compared to HepG2. Among these genes, DPP7 was the only one gene with HBV integration into its exon, meanwhile DPP7 expression level was also downregulated in HepG2.2.15 as compared to HepG2. Furthermore, DPP7 knockdown resulted in increased apoptosis through upregulation of the Bax/Bcl2 ratio in HepG2 cells. Our results suggest that HBV integration of DPP7 was involved in cell apoptosis.
Contents
Description
  • Site Information
Detail information of site [1019992]
  • Literature Information
The details of literature that this site is associated with.