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 Experiment Videos

Tumor-host interactions.

M J Tisdale1

  • 1Pharmaceutical Sciences Research Institute, Aston University, Birmingham, B4 7ET, United Kingdom. m.j.tisdale@aston.ac.uk

Journal of Cellular Biochemistry
|September 28, 2004
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

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

Sort by
Same author

The Green Tea Polyphenol Epigallocatechin-3-Gallate (EGCg) Attenuates Skeletal Muscle Atrophy in a Rat Model of Sarcopenia.

The Journal of frailty & aging·2016
Same author

Functional identity of receptors for proteolysis-inducing factor on human and murine skeletal muscle.

British journal of cancer·2014
Same author

Role of Ca2+ in proteolysis-inducing factor (PIF)-induced atrophy of skeletal muscle.

Cellular signalling·2012
Same author

Attenuation of muscle atrophy by an N-terminal peptide of the receptor for proteolysis-inducing factor (PIF).

British journal of cancer·2011
Same author

Studies on the anti-obesity activity of zinc-α2-glycoprotein in the rat.

International journal of obesity (2005)·2010
Same author

Studies on the antiobesity effect of zinc-α2-glycoprotein in the ob/ob mouse.

International journal of obesity (2005)·2010

Malignant tumors induce cancer cachexia through specific factors that disrupt host metabolism, leading to significant loss of muscle and fat tissue. These factors, including proteolysis-inducing factor (PIF) and lipid-mobilizing factor (LMF), alter protein synthesis and fat breakdown.

Area of Science:

  • Oncology
  • Metabolic Research
  • Biochemistry

Background:

  • Cancer cachexia is a complex syndrome involving significant loss of adipose and skeletal muscle mass.
  • While anorexia is common, nutritional deprivation alone does not fully explain the body composition changes in cancer cachexia.
  • Skeletal muscle mass loss results from decreased protein synthesis and increased protein degradation.

Purpose of the Study:

  • To elucidate the molecular mechanisms by which tumors induce cancer cachexia.
  • To identify the specific catabolic factors produced by tumors that affect host metabolism.
  • To understand the pathways involved in adipose tissue and skeletal muscle wasting.

Main Methods:

  • Analysis of protein synthesis and degradation pathways in skeletal muscle of cachectic patients.

Related Experiment Videos

  • Identification and characterization of tumor-derived catabolic factors like proteolysis-inducing factor (PIF).
  • Investigation of lipid metabolism alterations using lipid-mobilizing factor (LMF) and its interaction with cellular signaling pathways.

    • Main Results:

    • The ubiquitin-proteasome proteolytic pathway is upregulated in skeletal muscle of cachectic patients.
    • Proteolysis-inducing factor (PIF) produced by tumors inhibits protein synthesis and stimulates protein degradation in skeletal muscle.
    • Lipid-mobilizing factor (LMF), identified as Zn-alpha2-glycoprotein (ZAG), promotes triglyceride hydrolysis in adipose tissue.

    Conclusions:

    • Certain malignant tumors produce circulating factors that profoundly interfere with host metabolism, causing cancer cachexia.
    • Tumor-derived PIF and LMF are key mediators of skeletal muscle and adipose tissue loss, respectively.
    • Tumor-induced metabolic dysregulation occurs independently of metastatic site, highlighting systemic effects of cancer.