Ruan Xu Zhi, Yan Fei, Zhao Xin Yu, Wang Chung Ting, Song Ming, Yang Han Suo, Deng Hong Xin, Wei Yu Quan
State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, West China Medical School, Sichuan University, Ga-openg Street, Keyuan Road 4, Chengdu 610041, China.
Mol Cells. 2007 Jun 30;23(3):391-7.
FAM92A1 (named FAM92A1-271) belongs to the family of proteins with conserved DUF1208 domains. Its function remains elusive. We identified two novel transcript variants (FAM92A1-251, FAM92A1-289) of FAM92A1. The presence of these transcripts in cancerous and normal cells, as well as their influence on cell proliferation and apoptosis, were investigated. The subcellular location of FAM92A1 was determined by fluorescence microscopy. We found that FAM92A1-271 and FAM92A1- 289 were highly expressed in both normal and cancerous cells, but FAM92A1-251 was only expressed at a moderate level in both types of cell. Overexpression of FAM92A1-271, FAM92A1-251 and FAM92A1-289 inhibited cell proliferation, caused S-phase arrest and induced apoptosis. Subcellular localization showed that FAM92A1 localizes to the nucleus. Our results show that FAM92A1 has different splicing variants, and that it may take part in regulating cell proliferation and apoptosis.
FAM92A1(命名为FAM92A1-271)属于具有保守DUF1208结构域的蛋白质家族。其功能仍不清楚。我们鉴定出了FAM92A1的两种新型转录变体(FAM92A1-251、FAM92A1-289)。研究了这些转录本在癌细胞和正常细胞中的存在情况,以及它们对细胞增殖和凋亡的影响。通过荧光显微镜确定了FAM92A1的亚细胞定位。我们发现FAM92A1-271和FAM92A1-289在正常细胞和癌细胞中均高表达,但FAM92A1-251在这两种类型的细胞中仅中度表达。FAM92A1-271、FAM92A1-251和FAM92A1-289的过表达抑制细胞增殖,导致S期阻滞并诱导凋亡。亚细胞定位显示FAM92A1定位于细胞核。我们的结果表明FAM92A1具有不同的剪接变体,并且它可能参与调节细胞增殖和凋亡。