Roles of SALL2 in tumorigenesis

Abstract

The proteins p150^Sal2 (product of SALL2) and p53 share growth arrest and pro-apoptotic functions by independently inducing p21^Cip1/Waf1 and BAX, and both proteins are targeted by the human papilloma virus E6 protein, leading to blockage of growth arrest in infected cells. Loss of both p53 and Sall2 in mice causes significantly higher mortality and metastasis rates compared with p53 single mutant mice. Therefore, p150^Sal2 seems to have strong potential as a novel cancer biomarker for early diagnosis and risk prediction. Loss of SALL2 expression is observed in many cases of human serous ovarian carcinoma, whereas normal ovarian epithelial cells maintain high levels of the p150^Sal2 protein, supporting an important tumor suppressive role for p150^Sal2 in the human ovary. In contrast, p150^Sal2 is a transcription factor required to convert differentiated glioblastoma cells into stem-like tumor-propagating cells, suggesting that its functional roles are dependent on tissue types and cellular context. The function of p150^Sal2 in normal and diseased cells and possible therapeutic approaches are discussed in this review.

Keywords: BAX; Glioblastoma; Human papillomavirus; Mouse polyomavirus; Ovarian carcinoma; p150sal2; p21Cip1/Waf1; p53.