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

Mouse Models of Cancer Study02:43

Mouse Models of Cancer Study

Mice have long served as models for studying human biology and pathology because of their phylogenetic and physiological similarity with humans. They are also easy to maintain and breed in the laboratory, and hence, many inbred strains are now available for research. Studies on mice have contributed immeasurably to our understanding of cancer biology.
The development of transgenic, knockout, and knock-in mice has led to an exponential increase in their use as model organisms in research,...
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...
Animal Mitochondrial Genetics02:59

Animal Mitochondrial Genetics

Among all the organelles in an animal cell, only mitochondria have their own independent genomes. Animal mitochondrial DNA is a double-stranded, closed-circular molecule with around 20,000 base pairs. Mitochondrial DNA is unique in that one of its two strands, the heavy, or H, -strand is guanine rich, whereas the complementary strand is cytosine rich and called the light, or L, -strand. Compared to nuclear DNA, mitochondrial DNA has a very low percentage of non-coding regions and is marked by...
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...
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,...
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...

You might also read

Related Articles

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

Sort by
Same author

[Investigation of a causal relationship between mtDNA mutations and a mitochondrial respiratory dysfunction in premature aging mice].

Nihon yakurigaku zasshi. Folia pharmacologica Japonica·2026
Same author

Effects of an indole chemical, mitochonic acid 5, in a mouse model of mitochondrial disease onset.

Scientific reports·2026
Same author

Comparative analysis of muscle pathologies and metabolic signaling in mouse models of mitochondrial dysfunction.

Scientific reports·2026
Same author

Mitochondria-Dependent Metabolic Reprogramming Enhances Myofibroblast Differentiation and Aggravates Bleomycin-Induced Pulmonary Fibrosis.

Cells·2026
Same author

Mitochondrial vulnerability underlies myocarditis from COVID-19 mRNA vaccine.

Nature communications·2026
Same author

cGAS-IFN-I responses by extracting nuclear DNA from dying cells via nucleocytosis.

Nature communications·2026

Related Experiment Video

Updated: May 9, 2026

Transmitochondrial Cybrid Generation Using Cancer Cell Lines
07:49

Transmitochondrial Cybrid Generation Using Cancer Cell Lines

Published on: March 17, 2023

Polymorphic mutations in mouse mitochondrial DNA regulate a tumor phenotype.

Gaku Takibuchi1, Hirotake Imanishi, Mami Morimoto

  • 1Faculty of Life and Environmental Sciences, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8572, Japan.

Mitochondrion
|August 13, 2013
PubMed
Summary

Polymorphic mitochondrial DNA (mtDNA) mutations can influence tumor cell behavior and slow tumor growth. These findings are crucial for gene therapy considerations involving mtDNA replacement.

Keywords:
Hypoxia sensitivityMouse C3H mtDNAPolymorphic mtDNA mutationsTransmitochondrial cybridsTumor phenotypes

More Related Videos

Genotyping Single Nucleotide Polymorphisms in the Mitochondrial Genome by Pyrosequencing
07:24

Genotyping Single Nucleotide Polymorphisms in the Mitochondrial Genome by Pyrosequencing

Published on: February 10, 2023

A Genetically Engineered Mouse Model of Sporadic Colorectal Cancer
06:01

A Genetically Engineered Mouse Model of Sporadic Colorectal Cancer

Published on: July 6, 2017

Related Experiment Videos

Last Updated: May 9, 2026

Transmitochondrial Cybrid Generation Using Cancer Cell Lines
07:49

Transmitochondrial Cybrid Generation Using Cancer Cell Lines

Published on: March 17, 2023

Genotyping Single Nucleotide Polymorphisms in the Mitochondrial Genome by Pyrosequencing
07:24

Genotyping Single Nucleotide Polymorphisms in the Mitochondrial Genome by Pyrosequencing

Published on: February 10, 2023

A Genetically Engineered Mouse Model of Sporadic Colorectal Cancer
06:01

A Genetically Engineered Mouse Model of Sporadic Colorectal Cancer

Published on: July 6, 2017

Area of Science:

  • Mitochondrial genetics
  • Cancer biology
  • Cellular respiration

Background:

  • Polymorphic mitochondrial DNA (mtDNA) mutations are common.
  • The impact of non-respiratory-defect-inducing mtDNA mutations on tumor phenotypes is not fully understood.
  • Mitochondrial dysfunction is implicated in cancer development.

Purpose of the Study:

  • To investigate if polymorphic mtDNA mutations, without causing significant respiration defects, regulate tumor cell phenotypes.
  • To determine the effect of specific allogenic mtDNA on tumor cell behavior and growth.

Main Methods:

  • Utilized mouse transmitochondrial tumor cells (cybrids).
  • These cybrids possessed nuclear DNA from the C57BL/6 (B6) strain and mitochondrial DNA (mtDNA) from the allogenic C3H strain.
  • Tumorigenicity was assessed by subcutaneous inoculation into B6 mice.

Main Results:

  • Polymorphic mutations present in the C3H mtDNA within the cybrids induced hypoxia sensitivity.
  • This induced hypoxia sensitivity led to a delay in tumor formation after subcutaneous inoculation.
  • The presence of specific polymorphic mtDNA mutations altered tumor cell behavior.

Conclusions:

  • Polymorphic mtDNA mutations, even those not causing major respiration defects, can significantly influence tumor cell phenotypes.
  • The findings highlight the importance of considering the effects of polymorphic mutations in normal mtDNA.
  • Careful consideration is needed when applying gene therapy for mtDNA replacement, especially in embryonic contexts.