Physical activity counteracts tumor cell growth in colon carcinoma C26-injected muscles: an interim report

Hiroux, Charlotte; Vandoorne, Tijs; Koppo, Katrien; Smet, Stefan De; Hespel, Peter; Berardi, Emanuele

doi:10.4081/ejtm.2016.5958

Cited by 18 publications

(14 citation statements)

References 46 publications

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“…In addition, our observations on muscle denervation in cachexia could explain a previously reported subclinical myopathy in cancer patients, characterized by central nuclei in myofibers [24]. Since muscle regeneration is strongly inhibited in cachexia [20,[57][58][59], the central nuclei in cachectic muscles were so far unaccounted for, while our proposed model based on denervation could provide and explanation for this phenomenon (graphical abstract).…”

Section: Discussionmentioning

confidence: 60%

Displaced Myonuclei in Cancer Cachexia Suggest Altered Innervation

Daou

Hassani

Matos

et al. 2020

IJMS

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An idiopathic myopathy characterized by central nuclei in muscle fibers, a hallmark of muscle regeneration, has been observed in cancer patients. In cancer cachexia skeletal muscle is incapable of regeneration, consequently, this observation remains unaccounted for. In C26-tumor bearing, cachectic mice, we observed muscle fibers with central nuclei in the absence of molecular markers of bona fide regeneration. These clustered, non-peripheral nuclei were present in NCAM-expressing muscle fibers. Since NCAM expression is upregulated in denervated myofibers, we searched for additional makers of denervation, including AchRs, MUSK, and HDAC. This last one being also consistently upregulated in cachectic muscles, correlated with an increase of central myonuclei. This held true in the musculature of patients suffering from gastrointestinal cancer, where a progressive increase in the number of central myonuclei was observed in weight stable and in cachectic patients, compared to healthy subjects. Based on all of the above, the presence of central myonuclei in cancer patients and animal models of cachexia is consistent with motor neuron loss or NMJ perturbation and could underlie a previously neglected phenomenon of denervation, rather than representing myofiber damage and regeneration in cachexia. Similarly to aging, denervation-dependent myofiber atrophy could contribute to muscle wasting in cancer cachexia.

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Section: Discussionmentioning

confidence: 60%

Displaced Myonuclei in Cancer Cachexia Suggest Altered Innervation

Daou

Hassani

Matos

et al. 2020

IJMS

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“…There are published studies that show significant decrease in muscle mass in early and late stages of cancer progression that ultimately leads to a decrease in muscle function [ 47 – 50 ]. It has been observed that this process can be mediated through inflammation from presence of a tumor [ 47 , 48 ]. Interestingly, a recent study by Yu et al report that the compound ghrelin was shown to inhibit Dox-induced apoptosis in the gastrocnemius muscle, suggesting a therapeutic role in the associated cancer cachexia [ 51 ].…”

Section: Discussionmentioning

confidence: 99%

Secreted Frizzled‐Related Protein‐2 Inhibits Doxorubicin‐Induced Apoptosis Mediated through the Akt‐mTOR Pathway in Soleus Muscle

Merino

Singla

2018

Oxidative Medicine and Cellular Longevity

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Doxorubicin (Dox) is a potent chemotherapeutic drug known for its dose-dependent and serious adverse effects, such as cardiotoxicity and myotoxicity. Dox-induced cardiotoxicity (DIC) and muscle toxicity (DIMT) have been studied; however, the mechanisms of Dox-induced apoptosis in soleus muscle are not well defined. Our data shows that with Dox treatment, there is a significant increase in oxidative stress, apoptosis, proapoptotic protein BAX, pPTEN levels, and wnt3a and β-catenin activity (p < 0.05). Moreover, Dox treatment also resulted in decreased antioxidant levels, antiapoptotic BCL2, pAKT, p-mTOR, and endogenous levels of sFRP2 in the soleus muscle tissue (p < 0.05). Secreted frizzled-related protein 2 (sFRP2) treatment attenuated the adverse effects of DIMT and apoptosis in the soleus muscle, evidenced by a decrease in oxidative stress, apoptosis, BAX, pPTEN, and wnt3a and β-catenin activity, as well as an increase in antioxidants, BCL2, pAKT, p-MTOR, and sFRP2 levels (p < 0.05). This data suggests that Dox-induced oxidative stress and apoptosis is mediated through both the Akt-mTOR and wnt/β-catenin pathways. Moreover, the data also shows that sFRP2 modulates these two pathways by increasing signaling of Akt-mTOR and decreased signaling of the wnt/β-catenin pathway. Therefore, our data suggests that sFRP2 has valuable therapeutic potential in reversing Dox-induced oxidative stress and apoptosis in soleus muscle mediated through the Akt-mTOR pathway.

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“… 31 Beside pharmacological treatments, many studies including ours have established that exercise counteracts cachexia and sarcopenia. 32-35 The mechanisms underlying the beneficial effects of exercise against cachexia include autophagic flux regulation, 36 the reduction of Pax7 expression in satellite cells, 37 and the release of Hsp60 from muscle cells. 38 This topic was recently reviewed, 39-41 and it will be not further discussed here.…”

Section: Countermeasures: Would Exercise Be Effective Against Chemothmentioning

confidence: 99%

Chemotherapy-induced muscle wasting: an update

Coletti

2018

Eur J Transl Myol

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The majority of cancers are associated to cachexia, a severe form of weight loss mostly accounted for by skeletal muscle wasting. Cancer patients are often treated with chemotherapy, whose side effects are at times neglected or underestimated. Paradoxically, chemotherapy itself can induce muscle wasting with severe, cancer-independent effects on muscle homeostasis. Since muscle wasting is a primary marker of poor prognosis for cancer patients and negatively affects their quality of life, the systemic consequences of chemotherapy in this context must be fully characterized and taken into account. Ten years ago a precursor study in an animal cancer model was published in the European Journal of Translation Myology (back then, Basic and Applied Myology), highlighting that the side effects of chemotherapy include muscle wasting, possibly mediated by NF-κB activation. This paper, entitled «Chemotherapy-induced muscle wasting: association with NF-κB and cancer cachexia», is now being reprinted for the inaugural issue of the «Ejtm Seminal Paper Series». In this short review we discuss those results in the light of the most recent advances in the study of chemotherapy-induced muscle wasting.

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Physical activity counteracts tumor cell growth in colon carcinoma C26-injected muscles: an interim report

Cited by 18 publications

References 46 publications

Displaced Myonuclei in Cancer Cachexia Suggest Altered Innervation

Displaced Myonuclei in Cancer Cachexia Suggest Altered Innervation

Secreted Frizzled‐Related Protein‐2 Inhibits Doxorubicin‐Induced Apoptosis Mediated through the Akt‐mTOR Pathway in Soleus Muscle

Chemotherapy-induced muscle wasting: an update

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