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

Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

6.9K
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,...
6.9K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

4.6K
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...
4.6K
The Tumor Microenvironment02:17

The Tumor Microenvironment

7.6K
Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
7.6K

You might also read

Related Articles

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

Sort by
Same author

Synergistic Effect of Bimetallic Sites in Cu-Au Metallic Aerogels for Carbon Dioxide Electroreduction.

Chemphyschem : a European journal of chemical physics and physical chemistry·2026
Same author

Mechanical Activation of Piezo1 Drives Osteoarthritis Through Kdm5c-Mediated Epigenetic Silencing.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)·2026
Same author

Assessing drug-associated adverse events of spontaneous abortion or fetal death: A disproportionality analysis based on FDA adverse event reporting system.

Pakistan journal of pharmaceutical sciences·2026
Same author

Epidemiology, Phylogenetic Divergence, and Differential Pathogenicity of Feline Respiratory <i>Mycoplasma</i> in China.

Transboundary and emerging diseases·2026
Same author

Construction of a Lysine Lactylation- and DNA Damage Repair-Related Gene Signature to Predict the Prognosis and Drug Sensitivity of Breast Cancer Patients.

International journal of molecular sciences·2026
Same author

Heating- and leaching-free separation of electrodes by liquid metals for regeneration of spent Li-ion batteries.

National science review·2026

Related Experiment Video

Updated: Jan 12, 2026

Exploring the Regulation of Lipid Droplet Catabolism through Lipophagy
07:20

Exploring the Regulation of Lipid Droplet Catabolism through Lipophagy

Published on: January 31, 2025

1.1K

Cancer-associated adipocytes mediate CD8+T cell dysfunction via FGF21-driven lipolysis.

Sumiya Dalangood1, Cegui Hu1, Chenwei Yuan2

  • 1State Key Laboratory of Systems Medicine for Cancer, Ren Ji Hospital, Shanghai Cancer Institute, Shanghai Jiao Tong University School of Medicine, Shanghai 200127, China.

Cell Reports
|November 5, 2025
PubMed
Summary

Cancer-associated adipocytes release fatty acids, impairing CD8+ T cell function in tumors. Targeting this lipolysis, driven by FGF21 and ATGL, restores T cell activity and enhances cancer immunotherapy.

Keywords:
ATGLCD8(+)TCP: cancerCP: immunologyFGF21T cell exhaustioncancer-associated adipocyteslipolysistumor immunity

More Related Videos

Dual Effects of Melanoma Cell-derived Factors on Bone Marrow Adipocytes Differentiation
07:00

Dual Effects of Melanoma Cell-derived Factors on Bone Marrow Adipocytes Differentiation

Published on: August 23, 2018

6.5K
Modeling Breast Cancer in Human Breast Tissue using a Microphysiological System
10:51

Modeling Breast Cancer in Human Breast Tissue using a Microphysiological System

Published on: April 23, 2021

4.6K

Related Experiment Videos

Last Updated: Jan 12, 2026

Exploring the Regulation of Lipid Droplet Catabolism through Lipophagy
07:20

Exploring the Regulation of Lipid Droplet Catabolism through Lipophagy

Published on: January 31, 2025

1.1K
Dual Effects of Melanoma Cell-derived Factors on Bone Marrow Adipocytes Differentiation
07:00

Dual Effects of Melanoma Cell-derived Factors on Bone Marrow Adipocytes Differentiation

Published on: August 23, 2018

6.5K
Modeling Breast Cancer in Human Breast Tissue using a Microphysiological System
10:51

Modeling Breast Cancer in Human Breast Tissue using a Microphysiological System

Published on: April 23, 2021

4.6K

Area of Science:

  • Cancer biology
  • Immunology
  • Metabolic research

Background:

  • Cancer-associated adipocytes (CAAs) influence the tumor microenvironment (TME).
  • The metabolic interactions between CAAs and CD8+ T cells are not fully understood.
  • CD8+ T cells are crucial for anti-tumor immunity.

Purpose of the Study:

  • To investigate the metabolic crosstalk between CAAs and CD8+ T cells.
  • To identify mechanisms by which CAAs affect CD8+ T cell function.
  • To explore therapeutic strategies targeting CAA metabolism for cancer immunotherapy.

Main Methods:

  • Investigated lipolysis in CAAs and its impact on CD8+ T cells.
  • Utilized FGF21 deletion models and ATGL inhibition.
  • Assessed mitochondrial homeostasis and effector functions of CD8+ T cells.
  • Evaluated tumor growth and response to anti-PD-1 therapy.

Main Results:

  • CAAs release free fatty acids via lipolysis, causing lipid peroxidation and mitochondrial dysfunction in CD8+ T cells, leading to exhaustion.
  • FGF21 promotes CAA lipolysis by upregulating ATGL through FGFR1/KLB-p38 signaling.
  • FGF21 deletion or ATGL inhibition restored CD8+ T cell function and suppressed tumor growth.
  • Targeting CAA lipolysis enhanced anti-tumor immunity and efficacy of anti-PD-1 therapy.

Conclusions:

  • CAA lipolysis is a key mechanism of CD8+ T cell dysfunction in the TME.
  • Targeting CAA lipolysis, particularly FGF21/ATGL pathways, is a promising strategy to improve cancer immunotherapy.
  • Restoring CD8+ T cell effector function via metabolic reprogramming offers a novel therapeutic avenue.