Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2022 Apr 23;14(9):2107.
doi: 10.3390/cancers14092107.

Molecular Mechanisms and Current Treatment Options for Cancer Cachexia

Syed Sayeed Ahmad  1   2 , Khurshid Ahmad  1   2 , Sibhghatulla Shaikh  1   2 , Hye Jin You  3   4 , Eun-Young Lee  3 , Shahid Ali  2 , Eun Ju Lee  1   2 , Inho Choi  1   2
Affiliations
Review

Molecular Mechanisms and Current Treatment Options for Cancer Cachexia

Syed Sayeed Ahmad et al. Cancers (Basel). .

Abstract

Cancer cachexia is a condition marked by functional, metabolic, and immunological dysfunctions associated with skeletal muscle (SM) atrophy, adipose tissue loss, fat reduction, systemic inflammation, and anorexia. Generally, the condition is caused by a variety of mediators produced by cancer cells and cells in tumor microenvironments. Myostatin and activin signaling, IGF-1/PI3K/AKT signaling, and JAK-STAT signaling are known to play roles in cachexia, and thus, these pathways are considered potential therapeutic targets. This review discusses the current state of knowledge of the molecular mechanisms underlying cachexia and the available therapeutic options and was undertaken to increase understanding of the various factors/pathways/mediators involved and to identify potential treatment options.

Keywords: cancer cachexia; inhibitors; myostatin; natural compounds; skeletal muscle.

PubMed Disclaimer

Conflict of interest statement

The authors have no conflict of interest to declare.

Figures

Figure 1
Figure 1
The common assessment for the clinical management of cancer cachexia.
Figure 2
Figure 2
Molecular mechanisms regulated by IGF-1 and MSTN: Active Akt produces the mTOR signal, which leads to protein synthesis and inhibits (phosphorylates) FoxO. IGF-1 is primarily responsible for protein synthesis and muscle hypertrophy, whereas MSTN is responsible for protein degradation causing muscle atrophy. We suggest that screening of natural compounds and their derivatives for anti-MSTN activity might shift the balance toward muscle hypertrophy in cachexia.
See this image and copyright information in PMC

References

    1. Thibaut M.M., Sboarina M., Roumain M., Potgens S.A., Neyrinck A.M., Destree F., Gillard J., Leclercq I.A., Dachy G., Demoulin J.B., et al. Inflammation-induced cholestasis in cancer cachexia. J. Cachexia Sarcopenia Muscle. 2021;12:70–90. doi: 10.1002/jcsm.12652. - DOI - PMC - PubMed
    1. Tanaka K., Nakamura S., Narimatsu H. Nutritional Approach to Cancer Cachexia: A Proposal for Dietitians. Nutrients. 2022;14:345. doi: 10.3390/nu14020345. - DOI - PMC - PubMed
    1. Baracos V.E., Martin L., Korc M., Guttridge D.C., Fearon K.C.H. Cancer-associated cachexia. Nat. Rev. Dis. Primers. 2018;4:17105. doi: 10.1038/nrdp.2017.105. - DOI - PubMed
    1. Ohnuma T., Ali M.A., Adigun R. Anorexia and Cachexia. StatPearls; Treasure Island, FL, USA: 2021.
    1. Lee E.J., Jan A.T., Baig M.H., Ahmad K., Malik A., Rabbani G., Kim T., Lee I.K., Lee Y.H., Park S.Y., et al. Fibromodulin and regulation of the intricate balance between myoblast differentiation to myocytes or adipocyte-like cells. FASEB J. 2018;32:768–781. doi: 10.1096/fj.201700665R. - DOI - PubMed

LinkOut - more resources