More than 6 months of postoperative adjuvant chemotherapy results in loss of skeletal muscle: a challenge to the current standard of care

Kodera, Yasuhiro

doi:10.1007/s10120-014-0381-z

Cited by 19 publications

(15 citation statements)

References 7 publications

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“…It is worth noting that high-intensity physical exercise of athletes arouses systemic alteration in several biochemical states of skeletal muscle cells, including metabolic changes, ROS production, and consequent oxidative stress–induced muscle injury ( Cheng et al, 2020 ). Similarly, about 70%–80% of cancer patients experience muscle injury during chemotherapy, resulting in muscular functional impairments, sarcopenia, or even cachexia ( Kodera, 2015 ; Chen et al, 2016 ; Kakinuma et al, 2018 ; Matsuura et al, 2020 ). Potentially, chemotherapeutic drugs can induce ROS, resulting in muscle injury ( Kodera, 2015 ; Matsuura et al, 2020 ).…”

Section: Discussionmentioning

confidence: 99%

“…Similarly, about 70%–80% of cancer patients experience muscle injury during chemotherapy, resulting in muscular functional impairments, sarcopenia, or even cachexia ( Kodera, 2015 ; Chen et al, 2016 ; Kakinuma et al, 2018 ; Matsuura et al, 2020 ). Potentially, chemotherapeutic drugs can induce ROS, resulting in muscle injury ( Kodera, 2015 ; Matsuura et al, 2020 ). For example, cisplatin is widely used to combat multiple types of cancers, which is accompanied by side effects of inducing oxidative stress in muscle cells ( Sakai et al, 2014 ; Conte et al, 2020 ).…”

Section: Discussionmentioning

confidence: 99%

“…The inherent motion attribute of skeletal muscles is usually accompanied by the production of oxidative stress, which potentially results in myofiber damage upon untimely clearance ( Steinbacher and Eckl, 2015 ; Magherini et al, 2019 ; Cheng et al, 2020 ). Typically in cancer patients, some antineoplastic drugs exhibit high tendencies of muscle toxicity by inducing ROS production ( Kodera, 2015 ; Chen et al, 2016 ; Kakinuma et al, 2018 ; Matsuura et al, 2020 ). For example, cisplatin is a widely used chemotherapeutic drug with side effects including muscle weakness, muscle atrophy, or even cachexia.…”

Section: Introductionmentioning

confidence: 99%

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Taurine Protects C2C12 Myoblasts From Impaired Cell Proliferation and Myotube Differentiation Under Cisplatin-Induced ROS Exposure

Zhou

Huang

et al. 2021

Front. Mol. Biosci.

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In cancer patients, chemotherapeutic medication induces aberrant ROS (reactive oxygen species) accumulation in skeletal muscles, resulting in myofiber degradation, muscle weakness, and even cachexia, which further leads to poor therapeutic outcomes. Acting as an antioxidant, taurine is extensively used to accelerate postexercise muscle recovery in athletes. The antioxidant effects of taurine have been shown in mature myotubes and myofibers but not yet in myoblasts, the myotube precursor. The proliferation and differentiation ability of myoblasts play a very important role in myofiber repair and regeneration, which is usually impaired during chemotherapeutics in cancer patients as well. Here, we explored the effects of taurine supplementation on C2C12 myoblasts exposed to cisplatin-induced ROS. We found that cisplatin treatment led to dramatically decreased cell viability; accumulated ROS level; down-regulated expressions of MyoD1 (myoblast determination protein 1), myogenin, and MHC (myosin heavy chain); and impaired myotube differentiation in myoblasts. Significantly, taurine supplementation protected myoblasts against cisplatin-induced cell viability decrease, promoted cellular ROS clearance, and, most importantly, preserved the expressions of MyoD1, myogenin, and MHC as well as myotube differentiation ability. We further conducted NMR-based metabolomic analysis to clarify the underlying molecular mechanisms. We identified 14 characteristic metabolites primarily responsible for the discrimination of metabolic profiles between cisplatin-treated cells and normal counterparts, including increased levels of BCAAs (branched-chain amino acids: leucine and isoleucine), alanine, glycine, threonine, glucose, ADP (adenosine diphosphate), phenylalanine, and PC (O-phosphocholine), and decreased levels of lysine, β-alanine, choline, GPC (sn-glycero-3-phosphocholine), and myo-inositol. Evidently, taurine supplementation partially reversed the changing trends of several metabolites (isoleucine, threonine, glycine, PC, β-alanine, lysine, and myo-inositol). Furthermore, taurine supplementation promoted the proliferation and myotube differentiation of myoblasts by alleviating cellular catabolism, facilitating GSH (reduced glutathione) biosynthesis, improving glucose utilization and TCA (tricarboxylic acid) cycle anaplerosis, and stabilizing cellular membranes. Our results demonstrated the protective effects of taurine on cisplatin-impaired myoblasts and elucidated the mechanistic rationale for the use of taurine to ameliorate muscle toxicity in clinical chemotherapy cancer patients.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Taurine Protects C2C12 Myoblasts From Impaired Cell Proliferation and Myotube Differentiation Under Cisplatin-Induced ROS Exposure

Zhou

Huang

et al. 2021

Front. Mol. Biosci.

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“…A unique aspect of our study was the combined evaluation of skeletal muscle atrophy with appetite loss and gastric mucositis. The main mechanisms and causes underlying chemotherapy-induced muscle atrophy include (1) impaired food intake with reduction in vitamin D, (2) omega 3 fatty acids and protein, (3) reduced physical activity secondary to fatigue, (4) a direct effect of chemotherapy or targeted agents on muscle, and (5) malabsorption secondary to mucositis or treatment-related pancreatic insufficiency [ 31 ]. We previously reported a significant loss of skeletal muscle after completion of three-cycle cisplatin-based neoadjuvant chemotherapy in patients with muscle invasive bladder cancer [ 4 ].…”

Section: Discussionmentioning

confidence: 99%

Supplementary Oral Anamorelin Mitigates Anorexia and Skeletal Muscle Atrophy Induced by Gemcitabine Plus Cisplatin Systemic Chemotherapy in a Mouse Model

Miyake

Itami

Oda

et al. 2020

Cancers

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Chemotherapy-induced adverse effects can reduce the relative dose intensity and quality of life. In this study, we investigated the potential benefit of supplementary anamorelin and 5-aminolevulinic acid (5-ALA) as preventive interventions against a gemcitabine and cisplatin (GC) combination chemotherapy-induced adverse effects in a mouse model. Non-cancer-bearing C3H mice were randomly allocated as follows and treated for 2 weeks—(1) non-treated control, (2) oral anamorelin alone, (3) oral 5-ALA alone, (4) gemcitabine and cisplatin (GC) chemotherapy, (5) GC plus anamorelin, and (6) GC plus 5-ALA. GC chemotherapy significantly decreased body weight, food intake, skeletal muscle mass and induced severe gastric mucositis, which resulted in decreased ghrelin production and blood ghrelin level. The supplementation of oral anamorelin to GC chemotherapy successfully mitigated decrease of food intake during the treatment period and body weight loss at day 8. In addition, analysis of the resected muscles and stomach revealed that anamorelin suppressed chemotherapy-induced skeletal muscle atrophy by mediating the downregulation of forkhead box protein O-1 (FOXO1)/atrogin-1 signaling and gastric damage. Our findings suggest the preventive effect of anamorelin against GC combination chemotherapy, which was selected for patients with some types of advanced malignancies in clinical practice.

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“…Moreover, the stress hormones and inflammatory cytokines promote autophagy and mitochondrial dysfunction, which lead to muscle atrophy. These processes are regulated by atrogenes and transcription factors, such as NFκB and forkhead box protein O (FOXO).14 Especially in cancer patients, chemotherapy itself and malabsorption by complications of chemotherapy, such as mucositis, can directly induce muscle wasting [15].…”

Section: Alteration Of Energy Metabolism In Cancer Patientsmentioning

confidence: 99%

Nutritional issues in patients with cancer

Kim

2019

Intest Res

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Cachexia, commonly seen in cancer patients, is not simply caused by malnutrition due to anorexia. It is a more complex condition including reduced intake, metabolic dysfunction, and increased energy requirement. This process involves a va riety of inflammatory cytokines in cancer cells, alterations in protein and lipid metabolism, and an imbalance in the pro duction and degradation processes of muscle proteins. Dysfunction in the regulation of human inflammatory pro cess is observed in several diseases, including cancer. Resear ches have shown that increased inflammatory cytokines, such as TNFα and interleukin6 (IL6), play critical roles in the nu tritional metabolism of cancer patients. 4 TNFα is a cytokine related to cachexia, and it was originally called cachectin. 5 It has long been known that TNFα infusion causes loss of skele tal muscle mass in mice, and TNFα blocking immunoglobulin

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More than 6 months of postoperative adjuvant chemotherapy results in loss of skeletal muscle: a challenge to the current standard of care

Cited by 19 publications

References 7 publications

Taurine Protects C2C12 Myoblasts From Impaired Cell Proliferation and Myotube Differentiation Under Cisplatin-Induced ROS Exposure

Taurine Protects C2C12 Myoblasts From Impaired Cell Proliferation and Myotube Differentiation Under Cisplatin-Induced ROS Exposure

Supplementary Oral Anamorelin Mitigates Anorexia and Skeletal Muscle Atrophy Induced by Gemcitabine Plus Cisplatin Systemic Chemotherapy in a Mouse Model

Nutritional issues in patients with cancer

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