Sal-like protein 2 upregulates p16 expression through a proximal promoter element.
Bottom Line: Promoter-reporter assays of p16(INK4A) and several other tumor-related genes indicated that the Sall2 regulation of these promoters was not significantly different between the two major forms of Sall2 with alternative exon 1 or exon 1A.Finally, to confirm the significance of Sall2-activated p16 expression in cell cycle regulation, we co-transfected the SKOV3 cells with a Sall2 expression construct and a p16 minigene and also co-transfected the ES-2 cells with a Sall2 expression construct and the siRNA against p16 for flow cytometry analysis.Our results showed that Sall2 enhanced the p16 minigene blocking of cell cycle progression and p16 knockdown with siRNA abolished most of the Sall2 inhibition of cell cycle progression.
Affiliation: School of Pharmacy, Shanghai Jiao Tong University, Shanghai, China.Show MeSH
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Mentions: In order to find the Sall2 responsive binding site on p16 promoter, we constructed a series of p16 promoter mutants combining large segment deletions with specific deletions of some of the known transcription factor binding sites and analyzed the reporter luciferase activities in SKOV3 cells (Fig.4).
Affiliation: School of Pharmacy, Shanghai Jiao Tong University, Shanghai, China.