Genomic analysis of ovarian cancers demonstrated a regional chromosomal increase in expression and gene duplication. TGF-β stimulation indicated a link between SnoN RNA and TGF-β. In TIOSE, SnoN protein levels were reduced 15 min post TGF-β-stimulation, likely by proteosome-mediated degradation. SnoN inhibition decreased cell growth between 20 and 50% concurrent with increased p21 levels. Stable expression of SnoN led to growth arrest through induction of senescence. Collectively, these results implicate SnoN levels in multiple roles during ovarian carcinogenesis: promoting cellular proliferation in ovarian cancer cells and as a positive mediator of cell cycle arrest and senescence in non-transformed ovarian epithelial cells.
Nanjundan, Meera; Mills, Gordon; and Smith, Dawn, "Methods of treating ovarian cancer by modulating SnoN" (2012). USF Patents. 336.
University of South Florida