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

Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

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...
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 I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

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...
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...

You might also read

Related Articles

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

Sort by
Same author

Differentiation of Hemorrhage from Iodine Using Spectral Detector CT: A Phantom Study.

AJNR. American journal of neuroradiology·2018
Same author

Mechanosensitive Channels: Introduction.

The Biological bulletin·2017
Same author

Compact multichannel high-resolution micro-electro-mechanical systems-based interrogator for Fiber Bragg grating sensing.

Applied optics·2017
Same author

Performance of low-cost few-mode fiber Bragg grating sensor systems: polarization sensitivity and linearity of temperature and strain response.

Applied optics·2016
Same author

Inguinal Hernia: Crossfire Between the Meshes.

Hernia : the journal of hernias and abdominal wall surgery·2015
Same author

Mesh & Prosthesis.

Hernia : the journal of hernias and abdominal wall surgery·2015

Related Experiment Video

Updated: Jul 17, 2026

A Functional Assay for Gap Junctional Examination; Electroporation of Adherent Cells on Indium-Tin Oxide
11:02

A Functional Assay for Gap Junctional Examination; Electroporation of Adherent Cells on Indium-Tin Oxide

Published on: October 18, 2014

Gap-junction protein gene suppresses tumorigenicity

B Rose1, P P Mehta, W R Loewenstein

  • 1University of Miami School of Medicine, Department of Physiology and Biophysics, FL 33136.

Carcinogenesis
|May 1, 1993
PubMed
Summary

Introducing connexin43, a gap junction protein gene, into mouse cells restored normal cell communication and suppressed tumor growth. This highlights the role of cell-to-cell signaling in regulating cell proliferation and tumorigenesis.

More Related Videos

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

Removal of an Internal Translational Start Site from mRNA While Retaining Expression of the Full-Length Protein
05:48

Removal of an Internal Translational Start Site from mRNA While Retaining Expression of the Full-Length Protein

Published on: March 16, 2022

Related Experiment Videos

Last Updated: Jul 17, 2026

A Functional Assay for Gap Junctional Examination; Electroporation of Adherent Cells on Indium-Tin Oxide
11:02

A Functional Assay for Gap Junctional Examination; Electroporation of Adherent Cells on Indium-Tin Oxide

Published on: October 18, 2014

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

Removal of an Internal Translational Start Site from mRNA While Retaining Expression of the Full-Length Protein
05:48

Removal of an Internal Translational Start Site from mRNA While Retaining Expression of the Full-Length Protein

Published on: March 16, 2022

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • Gap junctions facilitate cell-to-cell communication through membrane channels.
  • These channels are hypothesized to transmit growth-regulating signals.
  • Tumorigenic cells often exhibit altered cell communication pathways.

Purpose of the Study:

  • To investigate the role of connexin43 in regulating cell growth and communication.
  • To determine if introducing connexin43 can restore normal growth regulation in tumorigenic cells.
  • To assess the impact of connexin43 expression on tumorigenicity.

Main Methods:

  • Gene transfer of rat connexin43 (alpha 1 gene) into mouse MCA-10 cells.
  • Confirmation of gene expression and functional channel formation.
  • Assessment of cell-cell communication using a fluorescent tracer.
  • Evaluation of tumorigenicity in nude mouse models.

Main Results:

  • Successful incorporation and expression of the exogenous connexin43 gene.
  • Restoration of functional gap junction channels.
  • Significant increase in cell-cell communication (measured by tracer permeability).
  • Suppression of tumor formation in vivo.

Conclusions:

  • Connexin43 expression restores normal cell-cell communication.
  • Gap junction-mediated signaling plays a critical role in suppressing tumorigenicity.
  • Gene transfer of connexin43 offers a potential strategy for cancer therapy.