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Myostatin expression in lung cancer induces sarcopenia and promotes cancer progression
Yo Kawaguchi1, Atsuko Watanabe2, Takuya Shiratori2
1Division of General Thoracic Surgery, Department of Surgery, Shiga University of Medical Science, Tsukinowacho, Seta, Otsu, Shiga, 520-2192, Japan. kawaguchi1228@yahoo.co.jp.
Objectives:
Many studies have demonstrated that sarcopenia among lung cancer predicts poor prognosis due to cancer progression. However, the cytokines that link sarcopenia and lung cancer progression remain unidentified. This study aimed to investigate whether lung cancer producing myostatin, which induces skeletal muscle atrophy, leads to sarcopenia and promotes cancer progression in patients with resected lung cancer.
Methods:
Tumor tissues were obtained from 148 patients who underwent curative resection for lung cancer. Tumor cells were stained with myostatin and tumor-associated macrophages (TAM) in the tumor microenvironment were stained with CD68. We assessed the association between myostatin expression and the clinicopathological features.
Results:
High myostatin expression in lung cancer was significantly associated with low skeletal muscle mass. The 5-year overall survival and relapse-free survival were significantly worse among patients with high myostatin expression than those with low expression. A multivariate analysis showed that TAM count was positively correlated with high myostatin expression.
Conclusion:
Sarcopenia may be induced by myostatin secreted by lung cancer cells. Moreover, myostatin may promote TAM migration into the tumor microenvironment, leading to advance lung cancer. As a result, patients with high myostatin expression had poor prognosis.
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