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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Format: | Theses |
Language: | Indonesia |
Online Access: | https://digilib.itb.ac.id/gdl/view/47236 |
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Institution: | Institut Teknologi Bandung |
Language: | Indonesia |
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.
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