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

The Ras Gene02:38

The Ras Gene

6.6K
The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a...
6.6K
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

9.3K
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...
9.3K
Abnormal Proliferation02:23

Abnormal Proliferation

4.7K
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...
4.7K
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

6.5K
Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
6.5K
Small GTPases - Ras and Rho01:24

Small GTPases - Ras and Rho

4.4K
Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
Three regulatory proteins control their activity:
4.4K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

3.9K
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...
3.9K

You might also read

Related Articles

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

Sort by
Same author

Identification of lysyl oxidase as an adipocyte-secreted mediator that promotes a partial mesenchymal-to-epithelial transition in MDA-MB-231 cells.

Exploration of targeted anti-tumor therapy·2024
Same author

The breast cancer microenvironment and lipoprotein lipase: Another negative notch for a beneficial enzyme?

FEBS open bio·2023
Same author

CD24 as a Potential Therapeutic Target in Patients with B-Cell Leukemia and Lymphoma: Current Insights.

OncoTargets and therapy·2022
Same author

Overview of the Maintenance of Authentic Cancer Cell Lines.

Methods in molecular biology (Clifton, N.J.)·2022
Same author

Culturing Suspension Cancer Cell Lines.

Methods in molecular biology (Clifton, N.J.)·2022
Same author

Three-Dimensional Co-Culture Method for Studying Interactions Between Adipocytes, Extracellular Matrix, and Cancer Cells.

Methods in molecular biology (Clifton, N.J.)·2022
Same journal

The effects of glutamine supplementation on inflammatory and oxidative stress indices in chronic diseases: a systematic review.

Amino acids·2026
Same journal

Reprogramming parasitic signatures into anticancer peptide candidates: in silico discovery of Leishmania major-derived peptides.

Amino acids·2026
Same journal

Effects of taurine on skeletal muscle in senescence-accelerated mice and C2C12 myoblasts and myotubes.

Amino acids·2026
Same journal

Dual functions of thermospermine in plant growth and stress responses.

Amino acids·2026
Same journal

Zinc finger protein-associated gene signature serves as a potential predictor for prognosis and therapeutic response in lung adenocarcinoma.

Amino acids·2026
Same journal

LC-MS assay for quantifying ornithine decarboxylase activity in the biological matrix and cultured cells using stable isotope‑labeled ornithine.

Amino acids·2026
See all related articles

Related Experiment Video

Updated: Oct 19, 2025

Focus Formation: A Cell-based Assay to Determine the Oncogenic Potential of a Gene
08:18

Focus Formation: A Cell-based Assay to Determine the Oncogenic Potential of a Gene

Published on: December 31, 2014

28.3K

Oncogenic Ras expression increases cellular formate production.

T Pongnopparat1, G Tingley1, Y Gao1

  • 1Department of Biochemistry, Memorial University of Newfoundland, St. John's, NL, Canada.

Amino Acids
|September 22, 2021
PubMed
Summary
This summary is machine-generated.

Oncogenic Ras (RasV12) significantly increases formate overflow in mouse fibroblasts, contributing to one-carbon unit production essential for cancer cell growth and proliferation.

Keywords:
CytosolFolateGlycineMethylenetetrahydrofolateMitochondriaSerine

More Related Videos

A Quantitative Measurement of Reactive Oxygen Species and Senescence-associated Secretory Phenotype in Normal Human Fibroblasts During Oncogene-induced Senescence
13:59

A Quantitative Measurement of Reactive Oxygen Species and Senescence-associated Secretory Phenotype in Normal Human Fibroblasts During Oncogene-induced Senescence

Published on: August 12, 2018

8.3K
Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants
07:38

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

Published on: June 6, 2025

359

Related Experiment Videos

Last Updated: Oct 19, 2025

Focus Formation: A Cell-based Assay to Determine the Oncogenic Potential of a Gene
08:18

Focus Formation: A Cell-based Assay to Determine the Oncogenic Potential of a Gene

Published on: December 31, 2014

28.3K
A Quantitative Measurement of Reactive Oxygen Species and Senescence-associated Secretory Phenotype in Normal Human Fibroblasts During Oncogene-induced Senescence
13:59

A Quantitative Measurement of Reactive Oxygen Species and Senescence-associated Secretory Phenotype in Normal Human Fibroblasts During Oncogene-induced Senescence

Published on: August 12, 2018

8.3K
Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants
07:38

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

Published on: June 6, 2025

359

Area of Science:

  • Biochemistry
  • Cell Biology
  • Oncology

Background:

  • One-carbon units are vital for cell growth, with formate production being a key pathway.
  • Elevated formate accumulation (formate overflow) is observed in oxidative cancers, but its cause is unclear.
  • Oncogenic signaling pathways are implicated in altered cellular metabolism during cancer development.

Purpose of the Study:

  • To investigate the impact of oncogenic Ras (RasV12) expression on formate production in NIH-3T3 fibroblasts.
  • To determine the metabolic origin of formate produced under RasV12 transformation.
  • To explore the correlation between RasV12 and the expression of enzymes involved in formate metabolism.

Main Methods:

  • NIH-3T3 fibroblasts were engineered to express oncogenic Ras (RasV12) or a control vector (Babe).
  • Cells were cultured with stable isotope-labeled 13C-serine or 13C-glycine to trace metabolic flux.
  • Formate accumulation and utilization rates were measured.
  • mRNA levels of enzymes involved in formate production were quantified.

Main Results:

  • RasV12-transformed fibroblasts exhibited a two-to-threefold increase in formate accumulation compared to control cells.
  • Formate production rates exceeded utilization rates in both cell types.
  • 13C-formate was predominantly derived from the #3 carbon of serine, with minimal labeling from glycine or serine #2 carbon.
  • Increased formate production correlated with elevated mRNA levels for key formate-producing enzymes in both mitochondrial and cytosolic compartments.

Conclusions:

  • Oncogenic RasV12 significantly enhances formate overflow in fibroblasts.
  • This RasV12-driven formate production represents a potential mechanism for supplying one-carbon units required for increased cancer cell proliferation.
  • The study highlights a metabolic adaptation induced by oncogenic signaling that supports tumor growth.