Effects of SASH1 on melanoma cell proliferation and apoptosis in vitro
Effects of SASH1 on melanoma cell proliferation and apoptosis in vitro
复制标题
SASH1对体外黑色素瘤细胞增殖和凋亡的影响
DOI：
10.3892/mmr.2012.1099
复制
发表时间：
2012-12-01
影响因子：
3.4
通讯作者：
He, Lin
中科院分区：
文献类型：
--
作者：
Lin, Sheyu;Zhang, Junyu;He, Lin
含有1的SAM和SH3结构域（SASH1）基因最初被发现是乳腺癌中潜在的肿瘤抑制基因，定位在染色体6q24.3上。SASH1的表达在人结肠癌中起预后作用。它的表达在几种人类恶性肿瘤中经常下调。然而，SASH1在黑色素瘤细胞中的生物学功能尚未确定。在本研究中，为了研究SASH I基因的抑瘤作用，我们建立了A-375稳定的黑色素瘤细胞系，过表达SASH I基因。采用增殖试验、凋亡试验、细胞周期分析和实时荧光定量PCR检测稳定细胞系。结果表明，SASH！来源于A-375细胞中的G2/M阻滞，并且Cdc2的磷酸化或细胞周期蛋白B-Cdc2结合的破坏可能是G2/M阻滞的原因。
The SAM and SH3 domain containing 1 (SASH1) gene was originally identified as a potential tumor suppressor gene in breast cancer, mapped on chromosome 6q24.3. The expression of SASH1 plays a prognostic role in human colon cancer. Its expression is frequently downregulated in several human malignancies. However, the biological function of SASH1 in melanoma cells is yet to be determined. In this study, in order to investigate the tumor suppressive effects of the SASH I gene, an A-375 stable melanoma cell line was established, overexpressing the SASH I gene. The stable cell line was examined using proliferation assay, apoptosis assay, cell cycle analysis and real-time PCR. The results indicated that the tumor suppressive activity of SASH! derived from G2/M arrest in A-375 cells, and that the phosphorylation of Cdc2 or the disruption of cyclin B-Cdc2 binding may be responsible for the G2/M arrest.