下调和上调
自噬
细胞生物学
信号转导
生物
表型
癌症研究
肌动蛋白细胞骨架
腺癌
肌动蛋白
细胞骨架
化学
癌症
细胞
基因
遗传学
细胞凋亡
作者
Yu Wang,Ran Zuo,Gengwei Huo,Zhiqiang Han,Yuchao He,Yi Luo,Liwei Chen,Guangtao Li,Jinfang Cui,Fuyi Zhu,Ping Yue,Dongqi Yuan,Yan Sun,Zhaoyue Li,Peng Chen,Hua Guo
标识
DOI:10.1096/fj.202300248r
摘要
Abstract Many studies have shown that the actin cytoskeleton plays an essential role in the initiation and progression of cancer. As an actin‐binding protein, Twinfilin1 (TWF1) plays an important role in regulating cytoskeleton‐related functions. However, little is known about the expression and function of TWF1 in human tumors. The present study aimed to investigate the functional roles and the underlying molecular mechanisms of TWF1 in human lung adenocarcinoma (LUAD). By using bioinformatics databases and tumor tissues, TWF1 expression was found to be higher in LUAD tissues than in adjacent tissues and poor survival was predicted in patients with LUAD. In vitro and in vivo assays indicated that downregulation of TWF1 expression suppressed LUAD cells invasion and migration. Further studies revealed that TWF1 interacted with p62 and was involved in the regulation of autophagy. The molecular mechanisms underlying TWF1 were investigated by RNA‐seq analysis and a series of functional experiments. The results showed that downregulation of TWF1 suppressed LUAD progression through the cAMP signaling pathway. Therefore, overexpression of TWF1 in LUAD promoted migration, invasion, and autophagy through the cAMP signaling pathway.
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