Related Experiment Video

Updated: May 24, 2026

Modeling Hepatitis B Virus Infection in Non-Hepatic 293T-NE-3NRs Cells
09:02

Modeling Hepatitis B Virus Infection in Non-Hepatic 293T-NE-3NRs Cells

Published on: June 5, 2020

XPD could suppress growth of HepG2.2.15 and down-regulate the expression of hepatitis B virus x protein through P53

Hao Ding1, Jiang-jing Xu, Yuan Huang

  • 1Department of Gastroenterology, Second Affiliated Hospital, Nanchang University, Nanchang, PR China.

Biochemical and Biophysical Research Communications
|March 6, 2012
PubMed
Abstract

Insights

Xeroderma pigmentosum D (XPD) suppresses hepatoma cell growth by regulating P53 pathway genes, including P21 and Bax. XPD

Area of Science:

  • Hepatocellular carcinoma research
  • Molecular oncology
  • DNA repair mechanisms

Background:

  • Hepatoma cell growth is complex and influenced by various proteins.
  • The role of Xeroderma pigmentosum D (XPD) in hepatocarcinogenesis is not fully understood.
  • The P53 pathway is a critical regulator of cell cycle and apoptosis in cancer.

Purpose of the Study:

  • To investigate the effect of XPD on hepatoma cell growth.
  • To analyze the impact of XPD on P21, Bax, Bcl-2, and Hepatitis B virus X protein (HBx) expression.
  • To determine if XPD influences these genes via the P53 pathway.

Main Methods:

  • Transfection of human hepatoma cells (HepG2.2.15) with XPD expression vector.
  • Inhibition of the P53 pathway using Pifithrin-α.
  • Analysis of gene expression (RT-PCR, Western blotting) and cell behavior (flow cytometry, MTT assay).

Main Results:

  • XPD overexpression increased P53, phospho-P53, P21, and Bax levels, while decreasing Bcl-2 and HBx.
  • XPD inhibited hepatoma cell viability and promoted apoptosis.
  • Inhibition of P53 abolished the effects of XPD on cell growth and apoptosis.

Conclusions:

  • XPD suppresses hepatoma cell growth by modulating P53 pathway targets P21, Bax, Bcl-2, and HBx.
  • XPD's influence on hepatocarcinogenesis may involve intricate interactions with P53 and HBx.
  • Targeting XPD could be a potential therapeutic strategy for hepatocellular carcinoma.

More Related Videos

Identifying Inhibitors of the HBx-DDB1 Interaction Using a Split Luciferase Assay System05:55

Identifying Inhibitors of the HBx-DDB1 Interaction Using a Split Luciferase Assay System

Published on: December 21, 2019

Development of a Hepatitis B Virus Reporter System to Monitor the Early Stages of the Replication Cycle09:35

Development of a Hepatitis B Virus Reporter System to Monitor the Early Stages of the Replication Cycle

Published on: February 1, 2017

Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
Cell Specific Gene Expression01:58

Cell Specific Gene Expression

Multicellular organisms contain a variety of structurally and functionally distinct cell types, but the DNA in all the cells originated from the same parent cells. The differences in the cells can be attributed to the differential gene expression. Liver cells, whose functions include detoxification of blood, production of bile to metabolize fats, and synthesis of proteins essential for metabolism, must express a specific set of genes to perform their functions. Gene expression also varies with...
Negative Regulator Molecules01:23

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.