Abstract
The transcription factor p150(Sal2), the product of the SALL2 gene, was first identified as a binding target of the oncogenic mouse polyomavirus T antigen. However, mouse polyomavirus is not the only oncogenic virus that targets p150(Sal2); the human papillomavirus E6 protein also targets this cellular protein in order to overcome p150(Sal2)-mediated growth arrest. Studies have demonstrated that p150(Sal2) recognizes GC-rich regions of the promoter and transcriptionally induces p21(Cip1/Waf1) and BAX in human ovarian epithelial cancer cells, resulting in cell growth arrest and apoptosis. Although the p150(Sal2) protein is strongly expressed in surface epithelial cells of the ovary, immunostaining experiments showed that expression of p150(Sal2) was lost in 90% of 210 human ovarian carcinomas, supporting an important tumor suppressive role for p150(Sal2) in the human ovary. Mechanisms of silencing SALL2 in OVCA cell lines and primary tumors and possible therapeutic approaches for ovarian carcinoma are discussed in this review.
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