Huang C C, Papas T S, Bhat N K
Center for Molecular and Structural Biology, Hollings Cancer Center, Medical University of South Carolina, Charleston 29425, USA.
Oncogene. 1997 Aug 14;15(7):851-6. doi: 10.1038/sj.onc.1201408.
We have previously shown that the human ETS1 protein (p51-ETS1), when ectopically expressed in colon cancer cell lines, is able to reduce its tumorigenicity without affecting its growth properties. To understand the mechanism of tumor reduction, we have expressed two different forms of ETS1 in colon cancer cell lines. Data presented in this paper indicate that the naturally occurring spliced variant protein, p42-ETS1, lacking the region encoded by ETS1 exon VII, represses the tumorigenicity, while p51-ETS1 reduces the tumorigenicity. Repression of tumorigenicity mediated by p42-ETS1 appears to be caused by its ability to induce apoptosis in epithelial cancer cells. This work can have profound medical significance in that it may open up new insights into the potential role of the p42-ETS1 in the induction of apoptosis in epithelial cell cancers and may provide a rationale for its use for potential gene therapy experiments to initiate cell death in cancer cells.
我们之前已经表明，人ETS1蛋白（p51-ETS1）在结肠癌细胞系中异位表达时，能够降低其致瘤性而不影响其生长特性。为了理解肿瘤减少的机制，我们在结肠癌细胞系中表达了两种不同形式的ETS1。本文呈现的数据表明，天然存在的剪接变体蛋白p42-ETS1，缺少由ETS1外显子VII编码的区域，可抑制致瘤性，而p51-ETS1则降低致瘤性。p42-ETS1介导的致瘤性抑制似乎是由其诱导上皮癌细胞凋亡的能力引起的。这项工作可能具有深远的医学意义，因为它可能为p42-ETS1在上皮细胞癌凋亡诱导中的潜在作用开辟新的见解，并可能为其用于潜在的基因治疗实验以引发癌细胞死亡提供理论依据。
