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

Covalently Linked Protein Regulators02:04

Covalently Linked Protein Regulators

6.9K
Proteins can undergo many types of post-translational modifications, often in response to changes in their environment. These modifications play an important role in the function and stability of these proteins. Covalently linked molecules include functional groups, such as methyl, acetyl, and phosphate groups, and also small proteins, such as ubiquitin. There are around 200 different types of covalent regulators that have been identified.
These groups modify specific amino acids in a protein....
6.9K
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
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

3.8K
The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
3.8K
Amplifying Signals via Enzymatic Cascade01:22

Amplifying Signals via Enzymatic Cascade

8.7K
When a ligand binds to a cell-surface receptor, the receptor's intracellular domain changes shape, which may either activate its enzyme function or allow its binding to other molecules. The initial signal is amplified by most signal transduction pathways. This means that a single ligand molecule can activate multiple molecules of a downstream target. Proteins that relay a signal are most commonly phosphorylated at one or more sites, activating or inactivating the protein. Kinases catalyze...
8.7K
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

6.4K
Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
6.4K
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

9.1K
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...
9.1K

You might also read

Related Articles

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

Sort by
Same author

Steatosis shapes prognosis-defining liver metastasis heterogeneity in CRC.

Nature·2026
Same author

Palmitoylation-mediated regulation of KAT2A promotes lung metastasis in breast cancer.

Nature cell biology·2026
Same author

A shift in the cellular redox state redirects aspartate for export under glucose deprivation.

Cancer & metabolism·2026
Same author

Author Correction: PHGDH heterogeneity potentiates cancer cell dissemination and metastasis.

Nature·2026
Same author

SILAC-based assessment of S-palmitoylated proteins in mammalian cells by metabolic labeling and click-chemistry.

Methods in cell biology·2025
Same author

HIF1α-dependent uncoupling of glycolysis suppresses tumor cell proliferation.

Cell reports·2024

Related Experiment Video

Updated: Aug 26, 2025

Utilizing a Comprehensive Immunoprecipitation Enrichment System to Identify an Endogenous Post-translational Modification Profile for Target Proteins
08:12

Utilizing a Comprehensive Immunoprecipitation Enrichment System to Identify an Endogenous Post-translational Modification Profile for Target Proteins

Published on: January 8, 2018

11.4K

Metabolite-derived protein modifications modulating oncogenic signaling.

Yawen Liu1,2,3, Anke Vandekeere2,3, Min Xu1

  • 1Department of Gastroenterology, Affiliated Hospital of Jiangsu University, Jiangsu University, Zhenjiang, China.

Frontiers in Oncology
|October 13, 2022
PubMed
Summary

Cancer growth involves metabolic changes, tumor suppressor inactivation, and oncogene activation. These processes intricately regulate each other, influencing cellular metabolism and protein modifications crucial for malignant progression.

Keywords:
metabolitesoncogenic signalingpost-translational modificationtumor microenvironmenttumor suppressor gene

More Related Videos

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants
07:39

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

Published on: June 6, 2025

227
SUMO-Binding Entities SUBEs as Tools for the Enrichment, Isolation, Identification, and Characterization of the SUMO Proteome in Liver Cancer
08:29

SUMO-Binding Entities SUBEs as Tools for the Enrichment, Isolation, Identification, and Characterization of the SUMO Proteome in Liver Cancer

Published on: November 1, 2019

7.2K

Related Experiment Videos

Last Updated: Aug 26, 2025

Utilizing a Comprehensive Immunoprecipitation Enrichment System to Identify an Endogenous Post-translational Modification Profile for Target Proteins
08:12

Utilizing a Comprehensive Immunoprecipitation Enrichment System to Identify an Endogenous Post-translational Modification Profile for Target Proteins

Published on: January 8, 2018

11.4K
Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants
07:39

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

Published on: June 6, 2025

227
SUMO-Binding Entities SUBEs as Tools for the Enrichment, Isolation, Identification, and Characterization of the SUMO Proteome in Liver Cancer
08:29

SUMO-Binding Entities SUBEs as Tools for the Enrichment, Isolation, Identification, and Characterization of the SUMO Proteome in Liver Cancer

Published on: November 1, 2019

7.2K

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Metabolism

Background:

  • Malignant growth is characterized by metabolic rewiring, tumor suppressor inactivation, and oncogene activation.
  • These hallmarks exhibit complex regulatory crosstalk, influencing each other's functions.

Purpose of the Study:

  • To summarize the interplay between tumor suppressors/oncogenes and metabolism-induced protein modifications.
  • To explore the impact of metabolic environments on these regulatory interactions.

Main Methods:

  • Review of existing literature on cancer hallmarks and metabolism.
  • Analysis of molecular mechanisms governing crosstalk between oncogenes, tumor suppressors, and metabolic pathways.

Main Results:

  • Aberrant cellular metabolism directly impacts oncogene and tumor suppressor activity.
  • Metabolic alterations and the tumor microenvironment modulate protein modifications of oncogenes and tumor suppressors at epigenetic and post-translational levels.

Conclusions:

  • The intricate crosstalk between cellular metabolism, oncogenes, and tumor suppressors is fundamental to malignant growth.
  • Metabolic (micro)environments play a critical role in shaping these regulatory networks, offering potential therapeutic targets.