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

6.7K
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,...
6.7K
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

7.9K
Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
7.9K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

4.5K
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...
4.5K
The Tumor Microenvironment02:17

The Tumor Microenvironment

7.5K
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...
7.5K
Cancer Cell Migration through Invadopodia01:35

Cancer Cell Migration through Invadopodia

3.0K
Invadosome is a broad category of cell surface structures with proteolytic activity that  degrades the extracellular matrix (ECM). Invadosomes are present in normal cell types, including macrophages, endothelial cells, and neurons, as well as tumor cells. Although the macrophage podosomes and tumor cell invadopodia are classified as invadosomes, they have different structures, molecular pathways, and functions. Podosomes are short structures that last for a few minutes. However,...
3.0K
Receptor Downregulation in MVBs01:15

Receptor Downregulation in MVBs

2.7K
Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that  lead to cell proliferation, migration, and differentiation. Overexpression of EGFR  stimulates cells to proliferate. Excessive  EGFR...
2.7K

You might also read

Related Articles

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

Sort by
Same author

A Dual-Action Gold(I) Prodrug Targeting Redox Homeostasis and Extracellular Matrix Remodeling in Ovarian Cancer.

ACS medicinal chemistry letters·2026
Same author

Senescent Stroma-Derived Glutamine: A Driver of Aggressiveness in Prostate and Ovarian Cancer Cells.

Cells·2026
Same author

Thiosugar-functionalized gold(I)-NHC complexes as selective anticancer agents for potential targeted therapy.

Frontiers in chemistry·2026
Same author

Ligand-Dependent DNA Binding and Cytotoxicity of Palladium(II) Complexes.

Chemistry (Weinheim an der Bergstrasse, Germany)·2025
Same author

Association Among Sperm Adiponectin, DNA Fragmentation, Oxidative Stress and Metabolites in Male Infertility.

Antioxidants (Basel, Switzerland)·2025
Same author

Oxaliplatin bioconjugates with human ferritin obtained by protein surface decoration: Characterization and biological evaluation.

Journal of inorganic biochemistry·2025

Related Experiment Video

Updated: Dec 15, 2025

The Colon-26 Carcinoma Tumor-bearing Mouse as a Model for the Study of Cancer Cachexia
08:55

The Colon-26 Carcinoma Tumor-bearing Mouse as a Model for the Study of Cancer Cachexia

Published on: November 30, 2016

16.9K

The Adipokines in Cancer Cachexia.

Michele Mannelli1, Tania Gamberi1, Francesca Magherini1

  • 1Department of Biomedical, Experimental and Clinical Sciences, University of Florence, Viale Morgagni 50, 50134 Florence, Italy.

International Journal of Molecular Sciences
|July 15, 2020
PubMed
Summary

Cancer cachexia involves significant weight loss due to muscle and fat depletion. Adipokines, hormones from fat tissue, are altered in cachexia, potentially offering new therapeutic targets.

Keywords:
adipokinesadipose tissuecancer cachexia

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

6.4K
Author Spotlight: Advanced Ex Vivo Model for Investigating Cancer-Adipose Microenvironment Interaction
05:42

Author Spotlight: Advanced Ex Vivo Model for Investigating Cancer-Adipose Microenvironment Interaction

Published on: January 26, 2024

3.0K

Related Experiment Videos

Last Updated: Dec 15, 2025

The Colon-26 Carcinoma Tumor-bearing Mouse as a Model for the Study of Cancer Cachexia
08:55

The Colon-26 Carcinoma Tumor-bearing Mouse as a Model for the Study of Cancer Cachexia

Published on: November 30, 2016

16.9K
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

6.4K
Author Spotlight: Advanced Ex Vivo Model for Investigating Cancer-Adipose Microenvironment Interaction
05:42

Author Spotlight: Advanced Ex Vivo Model for Investigating Cancer-Adipose Microenvironment Interaction

Published on: January 26, 2024

3.0K

Area of Science:

  • Endocrinology
  • Oncology
  • Metabolic Diseases

Background:

  • Cachexia, characterized by weight loss and muscle wasting, is a severe complication of diseases like cancer.
  • Adipose tissue plays a crucial role in overall health through adipokine secretion, influencing metabolic and differentiating processes.
  • Altered circulating adipokine levels are linked to insulin resistance, metabolic syndrome, diabetes, and cardiovascular disease.

Purpose of the Study:

  • To review the role of specific adipokines (leptin, adiponectin, resistin, apelin, visfatin) in cancer cachexia.
  • To highlight the potential of adipokines as therapeutic targets for cancer cachexia.

Main Methods:

  • Literature review of studies investigating adipokines in cancer cachexia.
  • Analysis of findings on altered circulating levels of adipokines in cachectic patients.

Main Results:

  • Cancer cachexia is associated with significant changes in adipokine secretion by adipose tissue.
  • Cachectic patients frequently exhibit altered levels of circulating adipokines.

Conclusions:

  • Adipokines are implicated in the pathology of cancer cachexia.
  • Further research into the involvement of adipokines could lead to novel therapeutic strategies for cancer cachexia.