缺失突变型 HBx 蛋白介导 PDK2 在肝细胞 肝癌中的差异表达及机制.

Objective To investigate the differential expression of PDK2 mediated by natural deletion mutant hepati‑ tis B virus X (HBx) protein in hepatocellular carcinoma (HCC), as well as the mechanism of long non-coding RNA (lncRNA) involved in regulation. Methods Huh7 cells were randomly divided into the empty vector group and HBx-128w group, and transfected with pcDNA3. 1 and pcDNA3. 1-HBx-128w, respectively. Western blotting was used to detect the expression of HBx protein in each group. LncRNA microarray was used to detect the stable transfected cells in the two groups, and the mRNA expression profiles and lncRNA expression profiles of Huh7 cells transfected with pcDNA3. 1-HBx128w were determined, and the differentially expressed genes were screened out. RT-qPCR was used to verify the results of lncRNA microarray in stable transfected cells. Bioinformatics was used to predict lncRNAs that might be involved in regulation, and RT-qPCR was used for verification in stable transfected cells. Results The lncRNA microarray results showed that PDK2 was up-regulated in Huh7 cells of HBx-128w group, and the fold change was 3. 219. RT-qPCR results showed that the concentration of PDK2 in Huh7 cells in the HBx-128w group was significantly higher than that in the pcDNA3. 1 group (P< 0. 05), and the fold change between the two groups was 3. 591. The expression level of lncRNA ENST0000511361 in HBx128w group was significantly higher than that in the pcDNA3.1 group (P<0. 05), and the fold change between the two groups was 3. 742. Conclusion PDK2 is up-regulated in Huh7 cells transfected with natural deletion mutant HBx-128w, and LncRNA ENST0000511361 may be involved in the regulation of PDK2 expression in the development of HCC. [ABSTRACT FROM AUTHOR]