Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Spatial mapping and senolytic targeting of senescent and disease-associated microglia in aged mouse brain white matter.

Nature aging·2026
Same author

Evidence for the Collective Nature of Radial Flow in Pb+Pb Collisions with the ATLAS Detector.

Physical review letters·2026
Same author

Evidence for the Dimuon Decay of the Higgs Boson in pp Collisions with the ATLAS Detector.

Physical review letters·2025
Same author

Evidence for Longitudinally Polarized W Bosons in the Electroweak Production of Same-Sign W Boson Pairs in Association with Two Jets in pp Collisions at sqrt[s]=13  TeV with the ATLAS Detector.

Physical review letters·2025
Same author

Observation of tt[over ¯] Production in Pb+Pb Collisions at sqrt[s_{NN}]=5.02  TeV with the ATLAS Detector.

Physical review letters·2025
Same author

Search for Dark Matter Produced in Association with a Dark Higgs Boson in the bb[over ¯] Final State Using pp Collisions at sqrt[s]=13  TeV with the ATLAS Detector.

Physical review letters·2025

Related Experiment Video

Updated: Jun 25, 2026

CD Spectroscopy to Study DNA-Protein Interactions
06:48

CD Spectroscopy to Study DNA-Protein Interactions

Published on: February 10, 2022

The SWI/SNF complex and cancer.

D Reisman1, S Glaros, E A Thompson

  • 1Department of Internal Medicine, University of Michigan College of Medicine, Ann Arbor, MI 48109-0686, USA. dreisman@med.umich.edu

Oncogene
|February 24, 2009
PubMed
Summary

Mammalian SWI/SNF complexes are vital for cell differentiation and proliferation. Evidence shows SWI/SNF components, particularly BRM and BRG1, act as tumor suppressors, with their loss linked to cancer.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • SWI/SNF complexes regulate ATP-dependent chromatin remodeling.
  • Chromatin remodeling is essential for cell differentiation and proliferation.
  • Dysregulation of SWI/SNF is implicated in malignant transformation.

Purpose of the Study:

  • To review the evidence supporting the tumor suppressor role of SWI/SNF components.
  • To highlight the roles of the catalytic subunits BRM and BRG1.

Main Methods:

  • Literature review of existing studies on SWI/SNF complexes.
  • Focus on genetic and functional evidence linking SWI/SNF to cancer.

Main Results:

  • Multiple SWI/SNF components function as tumor suppressors.

More Related Videos

Dissecting Multi-protein Signaling Complexes by Bimolecular Complementation Affinity Purification (BiCAP)
06:45

Dissecting Multi-protein Signaling Complexes by Bimolecular Complementation Affinity Purification (BiCAP)

Published on: June 15, 2018

Genome-Wide CRISPR Screen for Unveiling Radiosensitive and Radioresistant Genes
08:32

Genome-Wide CRISPR Screen for Unveiling Radiosensitive and Radioresistant Genes

Published on: May 23, 2025

Related Experiment Videos

Last Updated: Jun 25, 2026

CD Spectroscopy to Study DNA-Protein Interactions
06:48

CD Spectroscopy to Study DNA-Protein Interactions

Published on: February 10, 2022

Dissecting Multi-protein Signaling Complexes by Bimolecular Complementation Affinity Purification (BiCAP)
06:45

Dissecting Multi-protein Signaling Complexes by Bimolecular Complementation Affinity Purification (BiCAP)

Published on: June 15, 2018

Genome-Wide CRISPR Screen for Unveiling Radiosensitive and Radioresistant Genes
08:32

Genome-Wide CRISPR Screen for Unveiling Radiosensitive and Radioresistant Genes

Published on: May 23, 2025

  • BRM and BRG1 are key catalytic subunits with critical roles.

    • Conclusions:

    • Loss of SWI/SNF function contributes to cancer development.
    • BRM and BRG1 are significant tumor suppressors within the SWI/SNF family.