Related Experiment Video

Updated: Jul 13, 2026

Knockdown of FAM83A to Verify Its Role in Cervical Cancer Cell Growth and Cisplatin Sensitivity
04:20

Knockdown of FAM83A to Verify Its Role in Cervical Cancer Cell Growth and Cisplatin Sensitivity

Published on: February 9, 2024

Knock down of hSNF5/Ini1 causes cell cycle arrest and apoptosis in a p53-dependent manner

Hiroyuki Kato1, Reiko Honma, Takaomi Sanda

  • 1Department of Virology III, National Institute of Infectious Diseases, Musashimurayama, Tokyo, Japan. khiroyuki@imcb.a-star.edu.sg

Biochemical and Biophysical Research Communications
|August 3, 2007
PubMed

Insights

Loss of the hSNF5/Ini1 protein, crucial for the SWI/SNF complex, triggers a p53 signaling pathway. This leads to cell enlargement, G1 arrest, and apoptosis, potentially explaining rhabdoid tumor development.

Area of Science:

  • Molecular Biology
  • Oncology
  • Genetics

Background:

  • The SWI/SNF complex, involving hSNF5/Ini1, is vital in cellular processes.
  • Mutations in hSNF5/Ini1 are linked to aggressive pediatric rhabdoid tumors.
  • The molecular mechanisms driving rhabdoid tumor formation are not fully understood.

Purpose of the Study:

  • To investigate the functional consequences of hSNF5/Ini1 loss in HeLa cells.
  • To elucidate the molecular pathways activated by hSNF5/Ini1 suppression.
  • To explore the role of p53 and ARF in hSNF5/Ini1-deficient cells.

Main Methods:

  • HeLa cells were treated with siRNA to suppress hSNF5/Ini1 mRNA.
  • Gene expression profiling was performed using cDNA microarray analysis.
  • Protein levels and signaling pathways (p53, chk1/2, ARF) were assessed.

Main Results:

  • hSNF5/Ini1 suppression resulted in cell enlargement, G1 cell cycle arrest, and apoptosis.
  • Gene expression analysis revealed upregulation of p53-responsive genes, notably p21.
  • Enhanced p53 protein levels indicated activation of the p53 signaling pathway, independent of chk1/2.
  • Ectopic p14ARF expression induced similar cellular changes in ARF-deficient rhabdoid tumors.

Conclusions:

  • Loss of hSNF5/Ini1 activates a p53-dependent signaling pathway.
  • These findings provide insights into the molecular mechanisms underlying rhabdoid tumor pathogenesis.
  • The p53 and ARF pathways may play critical roles in hSNF5/Ini1-associated malignancies.

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

Preparation of Cell-lines for Conditional Knockdown of Gene Expression and Measurement of the Knockdown Effects on E4orf4-Induced Cell Death13:54

Preparation of Cell-lines for Conditional Knockdown of Gene Expression and Measurement of the Knockdown Effects on E4orf4-Induced Cell Death

Published on: October 21, 2012

Related Concept Videos

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...
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.
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 Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...