Related Experiment Video

Updated: Aug 23, 2026

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics
06:00

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics

Published on: May 14, 2016

ING4 induces G2/M cell cycle arrest and enhances the chemosensitivity to DNA-damage agents in HepG2 cells

Xin Zhang1, Lu-Sheng Xu, Zhi-Qin Wang

  • 1State Key Laboratory of Bioreactor Engineering, New World Institute of Biotechnology, East China University of Science and Technology, Shanghai 200237, China.

FEBS Letters
|July 15, 2004
PubMed

Insights

Inhibitor of growth 4 (ING4) overexpression halts cell growth and boosts apoptosis in HepG2 cells. ING4 enhances sensitivity to DNA-damaging chemotherapy agents, suggesting a role in cancer treatment.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • The inhibitor of growth (ING) gene family comprises candidate tumor suppressor genes.
  • ING4, a novel ING family member, interacts with tumor suppressors p53, p300, and NF-kappaB p65(RelA).

Purpose of the Study:

  • To investigate the cellular effects of exogenous ING4 expression in HepG2 cells.
  • To determine ING4's role in cell cycle regulation, apoptosis, and chemosensitivity.

Main Methods:

  • Overexpression of ING4 in HepG2 cells.
  • Cell cycle analysis (G2/M arrest).
  • Apoptosis assays triggered by serum starvation and DNA-damaging agents (etoposide, doxorubicin).
  • Western blot analysis for p21 and Bax expression in p53-proficient (HepG2) and p53-deficient (Saos-2) cells.

Main Results:

  • ING4 overexpression significantly inhibited HepG2 cell growth and induced G2/M cell cycle arrest.
  • ING4 enhanced apoptosis in HepG2 cells under serum starvation and increased cell death upon exposure to DNA-damage agents.
  • ING4 upregulated p21 and Bax in a p53-dependent manner, suggesting ING4-induced G2/M arrest is mediated by p21.

Conclusions:

  • ING4 functions as a tumor suppressor by inhibiting cell proliferation and promoting apoptosis.
  • ING4 enhances chemosensitivity to DNA-damaging agents in HepG2 cells, potentially through p53-dependent p21 upregulation.
  • ING4 represents a potential therapeutic target for enhancing cancer treatment efficacy.

More Related Videos

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols12:02

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols

Published on: June 6, 2017

Related Concept Videos

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.
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
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...
The Cell Cycle Control System01:28

The Cell Cycle Control System

The cell cycle regulation directs how a cell proceeds from one phase to the next and begins mitosis. The cell cycle control system includes intracellular regulatory molecules and external triggers. They provide "stop" or "advance" signals and operate at specific cell cycle stages termed checkpoints to ensure that a particular process is completed before the cell advances to the next phase.
Cyclins and cyclin-dependent kinases (Cdks) are the primary cell cycle regulators and function at the cell...