在小鼠胚胎成纤维细胞中，v-Src诱导的致癌转化需要SWAP-70。
SWAP-70 is required for oncogenic transformation by v-Src in mouse embryo fibroblasts.
作者信息
Fukui Yasuhisa, Tanaka Takayuki, Tachikawa Hiroyuki, Ihara Sayoko
机构信息
Division of Applied Biological Chemistry, Graduate School of Agricultural and Life Sciences, University of Tokyo, Bunkyo-ku, Tokyo 113-8657, Japan.
出版信息
Biochem Biophys Res Commun. 2007 May 4;356(2):512-6. doi: 10.1016/j.bbrc.2007.03.011. Epub 2007 Mar 8.
SWAP-70 is a phosphatidylinositol trisphosphate (PtdIns(3,4,5)P(3)) binding protein, which acts in F-actin rearrangement. The role of SWAP-70 in oncogenic transformation of mouse embryo fibroblasts (MEFs) by v-Src was examined by use of MEFs defective in SWAP-70. v-Src morphologically transformed MEFs lacking SWAP-70, but growth of the transformed cells in culture was slower than that of cells supplemented with exogenous SWAP-70. The v-Src-transformed MEFs deficient in SWAP-70 were unable to grow in soft agar while those expressing SWAP70 readily formed colonies, suggesting that SWAP-70 is required for anchorage independent growth of v-Src transformed MEFs. When transplanted in nude mice, tumors formed by the v-Src transformed SWAP-70(-/-) MEFs were smaller than those formed by cells expressing exogenous SWAP-70. These results suggest that SWAP-70 may be required for oncogenic transformation and contributes to cell growth in MEFs transformed by v-Src.
SWAP-70是一种磷脂酰肌醇三磷酸（PtdIns(3,4,5)P(3)）结合蛋白，作用于F-肌动蛋白重排。通过使用SWAP-70缺陷的小鼠胚胎成纤维细胞（MEF），研究了SWAP-70在v-Src诱导的小鼠胚胎成纤维细胞致癌转化中的作用。v-Src使缺乏SWAP-70的MEF发生形态转化，但转化细胞在培养中的生长速度比补充外源性SWAP-70的细胞慢。缺乏SWAP-70的v-Src转化的MEF在软琼脂中无法生长，而表达SWAP70的细胞则很容易形成集落，这表明SWAP-70是v-Src转化的MEF锚定非依赖性生长所必需的。当移植到裸鼠体内时，v-Src转化的SWAP-70(-/-)MEF形成的肿瘤比表达外源性SWAP-70的细胞形成的肿瘤小。这些结果表明，SWAP-70可能是致癌转化所必需的，并有助于v-Src转化的MEF中的细胞生长。
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