Abstract
AbstractCancer cachexia is characterized by irreversible muscle loss which is a critical factor in the prognosis of cancer patients. Myoblasts are myogenic precursor cells that are required to maintain skeletal muscle tissue. Previous studies have reported that cancer-released factors deteriorate myoblast differentiation, which is one of the causes of cachexia-associated muscle wasting. We recently identified the myogenetic oligodeoxynucleotide iSN04, which acts an anti-nucleolin aptamer and promotes myogenesis. The present study investigated the effects of iSN04 on human myoblasts exposed to conditioned medium (CM) of colon cancer cells. Cancer-CM impaired myogenic differentiation and myotube formation of myoblasts by upregulating the expression of inflammatory cytokines. iSN04 completely reversed cancer-CM-induced deteriorated myogenesis and inflammatory responses in myoblasts. Tumor necrosis factor-α (TNF-α), a representative cytokine present in cancer-CM, inhibited differentiation and induced inflammation of myoblasts, similar to cancer-CM. Pre-treatment with iSN04 reversed TNF-α-induced cachectic phenotypic features in myoblasts. These results indicate that iSN04 protects myoblasts against the effects of cancer-released factors and maintain their myogenic activity. This study provides a novel therapeutic strategy to prevent muscle loss associated with cancer cachexia.
Publisher
Cold Spring Harbor Laboratory
Cited by
2 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献