PI3K/AKT/mTOR通路
安普克
癌症研究
基因敲除
癌变
细胞生长
CD44细胞
生物
信号转导
细胞凋亡
细胞生物学
癌症
细胞
磷酸化
蛋白激酶A
生物化学
遗传学
作者
Zhong Wang,Zhanyong Zhu,Chenyuan Li,Yimin Zhang,Zhiyu Li,Shengrong Sun
标识
DOI:10.1016/j.yexcr.2020.112387
摘要
Non-muscle myosin IIA (NMIIA) has been reported to be involved in the carcinogenesis and malignant progression of various human tumors. However, the role and potential mechanism of NMIIA in the biological functions and apoptosis in colorectal cancer (CRC) remain elusive. In this study, we found that NMIIA was overexpressed in CRC tissues and significantly associated with poor survival in CRC patients. In addition, NMIIA promoted CRC cell proliferation and invasion via activating the AMPK/mTOR pathway in vitro, and NMIIA knockdown inhibited CRC growth in vivo. Meanwhile, NMIIA knockdown downregulated the CSCs markers (CD44 and CD133) expression in CRC cells. Furthermore, AMPK/mTOR pathway activation effectively reversed the NMIIA knockdown-induced inhibition of proliferation, invasion and stemness in CRC cells. Finally, NMIIA protects CRC cells from 5-FU-induced apoptosis and proliferation inhibition through the AMPK/mTOR pathway. Taken together, these results indicate that NMIIA plays a pivotal role in CRC growth and progression by regulating AMPK/mTOR pathway activation, and it may act as a novel therapeutic target prognostic factor in CRC.
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