A novel splice variant of supervillin, SV5, promotes carcinoma cell proliferation and cell migration

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• 作者：Xueran Chen^a ; ^b ; ¹ ; Haoran Yang^b ; ¹ ; Shangrong Zhang^a ; Zhen Wang^a ; Fang Ye^b ; Chaozhao Liang^a ; Hongzhi Wang^a ; ^b ; Zhiyou Fang^a ; ^b ; ^{z.fang@cmpt.ac.cn}
• 关键词：Supervillin ; Alternative splicing ; Cell proliferation ; Cell migration
• 刊名：Biochemical and Biophysical Research Communications
• 出版年：2017
• 出版时间：1 January 2017
• 年：2017
• 卷：482
• 期：1
• 页码：43-49
• 全文大小：1851 K
• 卷排序：482

文摘

Supervillin is an actin-associated protein that regulates actin dynamics by interacting with Myosin II, F-actin, and Cortactin to promote cell contractility and cell motility. Two splicing variants of human Supervillin (SV1 and SV4) have been reported in non-muscle cells; SV1 lacks 3 exons present in the larger isoform SV4. SV2, also called archvillin, is present in striated muscle; SV3, also called smooth muscle archvillin or SmAV, was cloned from smooth muscle. In the present study, we identify a novel splicing variant of Supervillin (SV5). SV5 contains a new splicing pattern. In the mouse tissues and cell lines examined, SV5 was predominantly expressed in skeletal and cardiac muscles and in proliferating cells, but was virtually undetectable in most normal tissues. Using RNAi and rescue experiments, we show here that SV5 displays altered functional properties in cancer cells, and regulates cell proliferation and cell migration.