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Updated: Sep 8, 2025
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The Colon-26 Carcinoma Tumor-bearing Mouse as a Model for the Study of Cancer Cachexia
Published on: November 30, 2016
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The mechanism by which noncoding RNAs regulate muscle wasting in cancer cachexia
Xueer Zhou1, Shoushan Hu1, Yunan Zhang1
1State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases & Dept. of Head and Neck Oncology, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, China.
Precision Clinical Medicine
|June 13, 2022
Summary
Cancer cachexia causes muscle wasting, but lacks diagnostics and cures. Extracellular vesicle-related noncoding RNAs are key players in muscle atrophy and may offer new therapeutic targets.
Area of Science:
- Biochemistry
- Molecular Biology
- Oncology
Background:
- Cancer cachexia (CC) is a metabolic syndrome causing significant muscle wasting in up to 80% of cancer patients.
- Current diagnostic methods and treatments for CC remain insufficient, despite extensive research into muscle atrophy mechanisms.
- Noncoding RNAs (ncRNAs) are increasingly recognized for their role in CC, influencing myogenesis inhibition and proteolysis activation.
Purpose of the Study:
- To review the role of noncoding RNAs (ncRNAs) transmitted via extracellular vesicles (EVs) in cancer cachexia.
- To summarize the mechanisms and targets of ncRNAs involved in CC-induced muscle atrophy.
- To highlight EV-related ncRNAs as potential therapeutic targets for cancer cachexia.
Main Methods:
- Literature review focusing on ncRNA transmission through EVs in the context of cancer cachexia.
- Analysis of studies investigating ncRNA expression profiles in cancer cachectic muscles.
- Examination of pathways and molecular targets implicated in ncRNA-mediated muscle wasting.
Main Results:
- Extracellular vesicles (EVs) act as crucial carriers for ncRNAs, mediating intercellular communication in cancer cachexia.
- Dysregulated ncRNA expression via EVs contributes to both the inhibition of muscle formation (myogenesis) and the breakdown of muscle protein (proteolysis).
- Specific ncRNAs and their pathways within EVs are identified as key drivers of muscle atrophy in CC.
Conclusions:
- EV-mediated ncRNA transfer plays a significant role in the pathogenesis of cancer cachexia-induced muscle wasting.
- Targeting EV-related ncRNAs presents a promising therapeutic strategy for combating muscle atrophy in cancer patients.
- Further research into these ncRNA pathways could lead to novel diagnostic and therapeutic interventions for CC.
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