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

Mutagenicity and Carcinogenicity01:25

Mutagenicity and Carcinogenicity

Mutagenicity and carcinogenicity refer to the ability of drugs to cause genetic defects and induce cancer, respectively. The International Agency for Research on Cancer (IARC) classifies agents into four groups based on their carcinogenic potential. Group 1 agents are known human carcinogens; group 2A agents are probably carcinogenic to humans; group 3 agents lack data to support their role in carcinogenesis; and group 4 includes agents for which data support that they are not likely to be...
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...
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,...
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...
Mutations01:39

Mutations

Overview
Tumor Progression02:07

Tumor Progression

Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...

You might also read

Related Articles

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

Sort by
Same author

Initial Psychometric Evaluation of the Social Safeness and Pleasure Scale Japanese Version.

Behavioral sciences (Basel, Switzerland)·2026
Same author

Guided internet-delivered compassion-focused therapy for women with recurrent pregnancy loss: A protocol of a randomized controlled trial.

PCN reports : psychiatry and clinical neurosciences·2026
Same author

Shared Origin of Y and Z Chromosomes in the Turnover of XY and ZW Systems in the Frog <i>Glandirana rugosa</i>.

Biomolecules·2026
Same author

Does compassion affect shame emotions and mental health in individuals with ASD traits.

BMC research notes·2026
Same author

Patient- and disease-specific factors associated with atrophy of the intrinsic muscles of the ulnar nerve in cubital tunnel syndrome.

Journal of orthopaedics·2026
Same author

XPR1 regulates fetal liver macrophage development, identity, and pyrenocyte clearance.

The Journal of experimental medicine·2025

Related Experiment Video

Updated: Jun 14, 2026

Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate (DMBA-TPA)
04:12

Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate (DMBA-TPA)

Published on: December 19, 2019

xCT deficiency accelerates chemically induced tumorigenesis.

Ami Nabeyama1, Ai Kurita, Kenichi Asano

  • 1Laboratory for Innate Cellular Immunity and Laboratory for Immunogenetics, RIKEN Research Center for Allergy and Immunology, Tsurumi, Yokohama, Kanagawa 230-0045, Japan.

Proceedings of the National Academy of Sciences of the United States of America
|March 24, 2010
PubMed
Summary

The xCT transporter is crucial for macrophage survival during inflammation by protecting against oxidative stress. Its deficiency impairs macrophage survival, leading to unremitting inflammation and accelerated tumor development.

More Related Videos

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer
28:15

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer

Published on: July 28, 2010

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen
19:44

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen

Published on: May 30, 2012

Related Experiment Videos

Last Updated: Jun 14, 2026

Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate (DMBA-TPA)
04:12

Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate (DMBA-TPA)

Published on: December 19, 2019

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer
28:15

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer

Published on: July 28, 2010

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen
19:44

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen

Published on: May 30, 2012

Area of Science:

  • Immunology
  • Cell Biology
  • Cancer Research

Background:

  • Macrophages are vital immune cells that combat inflammation but face oxidative stress.
  • The xCT transporter (part of system x(c)(-)) is upregulated in inflammatory sites and maintains intracellular glutathione for oxidative stress defense.
  • Impaired macrophage survival due to oxidative stress can lead to chronic inflammation and potentially cancer.

Purpose of the Study:

  • To investigate the role of the xCT transporter in macrophage survival and its impact on inflammation and tumorigenesis.
  • To determine if xCT deficiency exacerbates inflammation and tumor development.

Main Methods:

  • Generated a loss-of-function mouse mutant line (xCT(mu/mu)) using N-ethyl-N-nitrosourea mutagenesis.
  • Stimulated macrophages from wild-type and mutant mice with LPS to assess cell death and inflammatory markers.
  • Induced fibrosarcoma in mice using subcutaneous 3-methylcholanthrene (3-MCA) injection and analyzed tumor development and inflammatory cytokine expression in xCT(mu/mu) mice.

Main Results:

  • Macrophages from xCT(mu/mu) mice exhibited increased cell death and excessive release of high mobility group box chromosomal protein 1 upon LPS stimulation.
  • xCT deficiency resulted in impaired activated macrophage survival, leading to unremitting inflammation.
  • In xCT(mu/mu) mice, 3-MCA-induced fibrosarcoma development was accelerated, accompanied by overexpression of inflammatory cytokines like IL-1beta and TNFalpha.

Conclusions:

  • The xCT transporter is essential for protecting activated macrophages against oxidative stress and ensuring their survival at inflammatory sites.
  • Deficiency in the xCT-mediated protective system against oxidative stress impairs macrophage survival, exacerbates inflammation, and promotes tumor development.