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

Regulation of Metabolism01:19

Regulation of Metabolism

12.5K
Cellular needs and conditions vary from cell to cell and change within individual cells over time. For example, the required enzymes and energetic demands of stomach cells are different from those of fat storage cells, skin cells, blood cells, and nerve cells. Furthermore, a digestive cell works much harder to process and break down nutrients during the time that closely follows a meal compared with many hours after a meal. As these cellular demands and conditions vary, so do the amounts and...
12.5K
Epigenetic Regulation01:37

Epigenetic Regulation

4.3K
Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
X-chromosome...
4.3K
Epigenetic Regulation01:46

Epigenetic Regulation

26.4K
26.4K
Epigenetic Regulation01:46

Epigenetic Regulation

34.5K
Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
34.5K
Combination Therapies and Personalized Medicine02:50

Combination Therapies and Personalized Medicine

6.4K
Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...
6.4K
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

12.2K
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...
12.2K

You might also read

Related Articles

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

Sort by
Same author

Cuproptosis-immunity crosstalk informs strategy to overcome immunotherapy resistance.

Cell·2026
Same author

CD59 drives diet-induced obesity and glucose intolerance, insulin resistance, and metabolic dysfunction-associated steatotic liver disease.

npj metabolic health and disease·2026
Same author

Sex-based multiomics analysis uncovers metabolic and molecular mediators linking MASH and atherosclerosis.

JHEP reports : innovation in hepatology·2026
Same author

A metabolism-specific drug-repurposing screen reveals itraconazole as a potent OXPHOS inhibitor in acute myeloid leukemia.

Blood·2026
Same author

Targeting Oxalate Production by Combining Enzyme Inhibition and Proteolysis Activation: A Novel Therapeutic Approach for Primary Hyperoxaluria Type 1.

Journal of medicinal chemistry·2026
Same author

A step-by-step guide to performing cancer metabolism research using custom-made media.

Life science alliance·2025
Same journal

PDC1 deficiency results in 2-deoxyglucose sensitivity through inhibition of Pdc2 activity in yeast.

The FEBS journal·2026
Same journal

Epigenetic regulation of the hepcidin gene expression in hepatoma cells.

The FEBS journal·2026
Same journal

Loss of Ambp ameliorates steatosis progression by activating PPARα signaling in zebrafish.

The FEBS journal·2026
Same journal

Varying susceptibility of subpopulations along the epithelial-mesenchymal spectrum to undergo EMT.

The FEBS journal·2026
Same journal

ALOX15 links lipid metabolism to receptor trafficking in platelet activation.

The FEBS journal·2026
Same journal

A two-component ortholog of the Niemann-Pick C 1 protein is essential for normal growth and sterol trafficking and signaling in Tetrahymena thermophila.

The FEBS journal·2026
See all related articles

Related Experiment Video

Updated: Apr 15, 2026

Sequence-specific Labeling of Nucleic Acids and Proteins with Methyltransferases and Cofactor Analogues
12:07

Sequence-specific Labeling of Nucleic Acids and Proteins with Methyltransferases and Cofactor Analogues

Published on: November 22, 2014

14.5K

Oncometabolites: tailoring our genes.

Stefan Nowicki1, Eyal Gottlieb1

  • 1Cancer Research UK, Beatson Institute, Glasgow, UK.

The FEBS Journal
|April 14, 2015
PubMed
Summary
This summary is machine-generated.

Cancer cells utilize increased glucose metabolism and oncometabolites like succinate, fumarate, and 2-hydroxyglutarate to promote tumor growth by altering the epigenome. Targeting these oncometabolites offers future cancer treatment strategies.

Keywords:
cancerdioxygenaseepigeneticsmetabolismoncometabolites

More Related Videos

Author Spotlight: Characterizing Novel Enzymes from Extremophiles and Common Pathogens to Understand DNA Repair and Replication
05:33

Author Spotlight: Characterizing Novel Enzymes from Extremophiles and Common Pathogens to Understand DNA Repair and Replication

Published on: July 5, 2024

1.6K
An Engineered Split-TET2 Enzyme for Chemical-inducible DNA Hydroxymethylation and Epigenetic Remodeling
08:34

An Engineered Split-TET2 Enzyme for Chemical-inducible DNA Hydroxymethylation and Epigenetic Remodeling

Published on: December 18, 2017

7.1K

Related Experiment Videos

Last Updated: Apr 15, 2026

Sequence-specific Labeling of Nucleic Acids and Proteins with Methyltransferases and Cofactor Analogues
12:07

Sequence-specific Labeling of Nucleic Acids and Proteins with Methyltransferases and Cofactor Analogues

Published on: November 22, 2014

14.5K
Author Spotlight: Characterizing Novel Enzymes from Extremophiles and Common Pathogens to Understand DNA Repair and Replication
05:33

Author Spotlight: Characterizing Novel Enzymes from Extremophiles and Common Pathogens to Understand DNA Repair and Replication

Published on: July 5, 2024

1.6K
An Engineered Split-TET2 Enzyme for Chemical-inducible DNA Hydroxymethylation and Epigenetic Remodeling
08:34

An Engineered Split-TET2 Enzyme for Chemical-inducible DNA Hydroxymethylation and Epigenetic Remodeling

Published on: December 18, 2017

7.1K

Area of Science:

  • Biochemistry
  • Oncology
  • Epigenetics

Background:

  • Cancer cells exhibit increased glucose metabolism for growth and biosynthesis.
  • Oncometabolites, such as succinate, fumarate, and 2-hydroxyglutarate, are linked to tumorigenesis.
  • These oncometabolites arise from specific enzyme mutations and alter the epigenome.

Purpose of the Study:

  • To review the link between cellular metabolism and epigenetics in cancer.
  • To explore the role of oncometabolites in promoting tumorigenesis.
  • To discuss potential therapeutic strategies targeting oncometabolite-induced cancer.

Main Methods:

  • Literature review focusing on the relationship between metabolism and epigenetics.
  • Analysis of the role of specific oncometabolites (succinate, fumarate, 2-hydroxyglutarate).
  • Discussion of α-ketoglutarate-dependent dioxygenases and their inhibition by oncometabolites.

Main Results:

  • Oncometabolites promote tumor growth by altering epigenetic modifications.
  • Structural similarity of oncometabolites to α-ketoglutarate enables competitive inhibition of key enzymes.
  • These enzymes are crucial for processes including gene expression regulation via demethylation.

Conclusions:

  • Oncometabolites represent a critical link between cancer metabolism and epigenetic dysregulation.
  • Targeting oncometabolites and their downstream effects presents a promising avenue for cancer therapy.
  • Understanding these metabolic-epigenetic interactions is key to developing novel anti-cancer treatments.