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

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...
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
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...
Epigenetic Regulation01:46

Epigenetic Regulation

Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.

You might also read

Related Articles

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

Sort by
Same author

KIF14 silencing suppresses cell proliferation and enhances chemosensitivity by modulating 53BP1 nucleocytoplasmic shuttling in non-WNT/non-SHH medulloblastoma.

Cell death discoveryยท2026
Same author

Joint effects of visual acuity impairment and visual field loss on reading performance: a low-vision simulation in Chinese readers.

Eye and vision (London, England)ยท2026
Same author

Glutathione-Induced In Situ Oxygen Vacancies in FeOOH Nanospindles for Boosting Sonocatalytic Tumor Therapy.

Angewandte Chemie (International ed. in English)ยท2026
Same author

Publisher Correction: Multi-ancestry genome-wide association analyses of refractive error augment genetic discovery and polygenic prediction.

Nature geneticsยท2026
Same author

Directly Encrypting DNA Sequences for Secure DNA Storage via Automata Cryptography.

IEEE transactions on nanobioscienceยท2026
Same author

Quantum-Enhanced Dark Matter Search Using Cat States.

Physical review lettersยท2026

Related Experiment Video

Updated: Jun 7, 2026

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells
09:37

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells

Published on: August 25, 2021

FOXP3 as an X-linked tumor suppressor.

Lizhong Wang1, Runhua Liu, Mark Ribick

  • 1Division of Immunotherapy, Department of Surgery, University of Michigan School of Medicine and Cancer Center, Ann Arbor, Michigan 48109, USA. lizhongw@umich.edu

Discovery Medicine
|November 2, 2010
PubMed
Summary

The FOXP3 gene, linked to autoimmune diseases, also plays a role in mammary and prostate tumors. Its selective inactivation in cancer suggests a potential therapeutic strategy for reactivation.

More Related Videos

Identification of OTX1 and OTX2 As Two Possible Molecular Markers for Sinonasal Carcinomas and Olfactory Neuroblastomas
07:00

Identification of OTX1 and OTX2 As Two Possible Molecular Markers for Sinonasal Carcinomas and Olfactory Neuroblastomas

Published on: February 28, 2019

Related Experiment Videos

Last Updated: Jun 7, 2026

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells
09:37

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells

Published on: August 25, 2021

Identification of OTX1 and OTX2 As Two Possible Molecular Markers for Sinonasal Carcinomas and Olfactory Neuroblastomas
07:00

Identification of OTX1 and OTX2 As Two Possible Molecular Markers for Sinonasal Carcinomas and Olfactory Neuroblastomas

Published on: February 28, 2019

Area of Science:

  • Genetics
  • Oncology
  • Immunology

Background:

  • The FOXP3 gene is crucial for immune regulation and was initially identified due to its role in lethal autoimmune diseases.
  • Mutations in the FOXP3 gene (or its mouse homolog, FoxP3) are associated with spontaneous mammary tumors in mice and prostate intraepithelial neoplasia.
  • Somatic mutations, deletions, and epigenetic silencing of FOXP3 are frequently observed in human breast and prostate cancers.

Purpose of the Study:

  • To investigate the role of the FOXP3 gene in the development of mammary and prostate cancers.
  • To explore the mechanism of FOXP3 inactivation in cancer, particularly its X-linked nature.
  • To identify potential therapeutic strategies based on FOXP3's function in cancer.

Main Methods:

  • Analysis of FOXP3 gene status (mutations, deletions, epigenetic inactivation) in human breast and prostate cancer samples.
  • Comparison of FOXP3 inactivation patterns in cancer with those of autosomal tumor suppressor genes.
  • Investigation of X-chromosome inactivation patterns in cancer cells with FOXP3 mutations.

Main Results:

  • FOXP3 inactivation is widespread in human breast and prostate cancers.
  • Unlike autosomal tumor suppressors, FOXP3 inactivation in cancer is typically heterozygous.
  • Evidence of selective inactivation of the wildtype FOXP3 allele in cancer cells, suggesting skewed X-inactivation.

Conclusions:

  • The FOXP3 gene functions as a tumor suppressor in mammary and prostate tissues.
  • Skewed X-inactivation leading to selective loss of functional FOXP3 is a key mechanism in these cancers.
  • Reactivation of FOXP3 presents a novel therapeutic avenue for treating breast and prostate cancers.