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Muscle wasting assessment tools for prostate cancer.

ABSTRACT: Prostate cancer and its treatment may induce muscle wasting. Body composition and muscle functionality are rarely assessed in patients with prostate cancer from developing countries due to the limited availability of high-quality equipment for routine diagnosis. This cross-sectional study evaluated the association between several simplistic techniques for assessing muscle mass and function with a more complex standard of reference for muscle wasting among Mexican men with prostate cancer. Muscle wasting was highly prevalent, yet it was presumably associated with aging rather than cancer and its treatment itself. The restricted availability of specific equipment in clinical settings with technological limitations supports using unsophisticated techniques as surrogate measurements for muscle wasting. The left-arm handgrip dynamometry displayed the highest correlation with the standard of reference and exhibited an acceptable predicted probability for muscle estimation. Combining several simplistic techniques may be preferable. We also developed and internally validated a manageable model that helps to identify elderly patients with prostate cancer at risk of muscle depletion and impairment. These findings promote the early recognition and treatment of muscle wasting alterations occurring among older adults with prostate cancer.

SUBMITTER: Espinosa-Marron A

PROVIDER: S-EPMC8933481 | biostudies-literature | 2022 Mar

REPOSITORIES: biostudies-literature

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Muscle wasting assessment tools for prostate cancer.

Espinosa-Marrón Alan A Rubio-Blancas Aquiles A Quiñones-Capistran Christian Aníbal CA Camacho-Zamora Anais A Salcedo-Grajales Itzel I Bravo-García Ana Paula AP Bourlon Maria T MT Castillejos-Molina Ricardo A RA Dias Julie-Alexia JA Del Pilar Milke-García María M

Scientific reports 20220318 1

Prostate cancer and its treatment may induce muscle wasting. Body composition and muscle functionality are rarely assessed in patients with prostate cancer from developing countries due to the limited availability of high-quality equipment for routine diagnosis. This cross-sectional study evaluated the association between several simplistic techniques for assessing muscle mass and function with a more complex standard of reference for muscle wasting among Mexican men with prostate cancer. Muscle ...[more]

PMID: 35304535

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Project description:BackgroundCancer-related muscle wasting occurs in most cancer patients. An important regulator of adult muscle mass and function is the Akt-mTORC1 pathway. While Akt-mTORC1 signalling is important for adult muscle homeostasis, it is also a major target of numerous cancer treatments. Which role Akt-mTORC1 signalling plays during cancer cachexia in muscle is currently not known. Here, we aimed to determine how activation or inactivation of the pathway affects skeletal muscle during cancer cachexia.MethodsWe used inducible, muscle-specific Raptor ko (mTORC1) mice to determine the effect of reduced mTOR signalling during cancer cachexia. On the contrary, in order to understand if skeletal muscles maintain their anabolic capacity and if activation of Akt-mTORC1 signalling can reverse cancer cachexia, we generated mice in which we can inducibly activate Akt specifically in skeletal muscles.ResultsWe found that mTORC1 signalling is impaired during cancer cachexia, using the Lewis lung carcinoma and C26 colon cancer model, and is accompanied by a reduction in protein synthesis rates of 57% (P < 0.01). Further reduction of mTOR signalling, as seen in Raptor ko animals, leads to a 1.5-fold increase in autophagic flux (P > 0.001), but does not further increase muscle wasting. On the other hand, activation of Akt-mTORC1 signalling in already cachectic animals completely reverses the 15-20% loss in muscle mass and force (P < 0.001). Interestingly, Akt activation only in skeletal muscle completely normalizes the transcriptional deregulation observed in cachectic muscle, despite having no effect on tumour size or spleen mass. In addition to stimulating muscle growth, it is also sufficient to prevent the increase in protein degradation normally observed in muscles from tumour-bearing animals.ConclusionsHere, we show that activation of Akt-mTORC1 signalling is sufficient to completely revert cancer-dependent muscle wasting. Intriguingly, these results show that skeletal muscle maintains its anabolic capacities also during cancer cachexia, possibly giving a rationale behind some of the beneficial effects observed in exercise in cancer patients.

Project description:BackgroundCachexia, a multifactorial syndrome affecting more than 50% of patients with advanced cancer and responsible for ~20% of cancer-associated deaths, is still a poorly understood process without a standard cure available. Skeletal muscle atrophy caused by systemic inflammation is a major clinical feature of cachexia, leading to weight loss, dampening patients' quality of life, and reducing patients' response to anticancer therapy. RAGE (receptor for advanced glycation end-products) is a multiligand receptor of the immunoglobulin superfamily and a mediator of muscle regeneration, inflammation, and cancer.MethodsBy using murine models consisting in the injection of colon 26 murine adenocarcinoma (C26-ADK) or Lewis lung carcinoma (LLC) cells in BALB/c and C57BL/6 or Ager-/- (RAGE-null) mice, respectively, we investigated the involvement of RAGE signalling in the main features of cancer cachexia, including the inflammatory state. In vitro experiments were performed using myotubes derived from C2C12 myoblasts or primary myoblasts isolated from C57BL/6 wild type and Ager-/- mice treated with the RAGE ligand, S100B (S100 calcium-binding protein B), TNF (tumor necrosis factor)α±IFN (interferon) γ, and tumour cell- or masses-conditioned media to analyse hallmarks of muscle atrophy. Finally, muscles of wild type and Ager-/- mice were injected with TNFα/IFNγ or S100B in a tumour-free environment.ResultsWe demonstrate that RAGE is determinant to activate signalling pathways leading to muscle protein degradation in the presence of proinflammatory cytokines and/or tumour-derived cachexia-inducing factors. We identify the RAGE ligand, S100B, as a novel factor able to induce muscle atrophy per se via a p38 MAPK (p38 mitogen-activated protein kinase)/myogenin axis and STAT3 (signal transducer and activator of transcription 3)-dependent MyoD (myoblast determination protein 1) degradation. Lastly, we found that in cancer conditions, an increase in serum levels of tumour-derived S100B and HMGB1 (high mobility group box 1) occurs leading to chronic activation/overexpression of RAGE, which induces hallmarks of cancer cachexia (i.e. muscle wasting, systemic inflammation, and release of tumour-derived pro-cachectic factors). Absence of RAGE in mice translates into reduced serum levels of cachexia-inducing factors, delayed loss of muscle mass and strength, reduced tumour progression, and increased survival.ConclusionsRAGE is a molecular determinant in inducing the hallmarks of cancer cachexia, and molecular targeting of RAGE might represent a therapeutic strategy to prevent or counteract the cachectic syndrome.

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Muscle wasting assessment tools for prostate cancer.

Publications

Muscle wasting assessment tools for prostate cancer.

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