THE EFFECT OF HEPATITIS B VIRUS X PROTEIN MUTANT T118N AND K130M/V131I ON APOPTOSIS, CELL CYCLE, AND TRANSCRIPTOME PROFILE OF HEPG2 CELLS

Hepatitis B virus (HBV) is a major cause of liver cirrhosis which could develop into liver carcinoma. HBV X protein (HBx) is known to have a role in the pathogenesis of liver carcinoma caused by HBV. Mutations in gene x affect the functional mechanism of HBx and play a role in the development of...

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Bibliographic Details
Main Author: Rizky Gilang Mahaputra, Andhika
Format: Theses
Language:Indonesia
Online Access:https://digilib.itb.ac.id/gdl/view/47236
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Institution: Institut Teknologi Bandung
Language: Indonesia
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Summary:Hepatitis B virus (HBV) is a major cause of liver cirrhosis which could develop into liver carcinoma. HBV X protein (HBx) is known to have a role in the pathogenesis of liver carcinoma caused by HBV. Mutations in gene x affect the functional mechanism of HBx and play a role in the development of chronic hepatitis B into liver carcinoma. The purpose of this study is to determine the effect of HBx T118N and K130M/V131I on apoptosis and cell cycle in HepG2 cells using the flow cytomery and to determine the transcriptome profile of HepG2 cells using Next Generation Sequencing (NGS). Apoptosis, cell cycle, and transcriptome profile of HepG2 cells were observed by comparing the effect of HBx T118N and HBx K130M/V131I to HBx wild-type. The results of apoptosis analysis showed a decrease in apoptosis in HepG2 cells expressing HBx K130M/V131I and increased apoptosis in HepG2 cells expressing HBx T118N in the early apoptosis and late apoptosis, as compared to HepG2 cells expressing HBx wild-type. The results of cell cycle analysis showed no difference in the cell cycle regulation of HepG2 cells expressing HBx wild-type, HBx K130M/V131I, and HBx T118N. Transcriptomic analysis using NGS showed upregulation in the hspa6 gene and downregulation in the rna28s5 gene. Both genes are known to play a role in apoptosis and cell cycle regulation.