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Methods of treating ovarian cancer by modulating SnoN

United States Patent

July 3, 2012
View the Complete Patent at the US Patent & Trademark Office
Lawrence Berkeley National Laboratory - Visit the Technology Transfer and Intellectual Property Management Department Website
Genomic analysis of ovarian cancers demonstrated a regional chromosomal increase in expression and gene duplication. TGF-.beta. stimulation indicated a link between SnoN RNA and TGF-.beta.. In TIOSE, SnoN protein levels were reduced 15 min post TGF-.beta.-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 (Tampa, FL), Mills; Gordon (Houston, TX), Smith; Dawn (Polk City, FL)
University of South Florida (Tampa, FL)
12/ 619,345
November 16, 2009
GOVERNMENT SUPPORT STATEMENT This invention was made with government support under Grant Nos. CA123219-01A2, CA083639, CA16672 and CA64602, awarded by the National Cancer Institute, RO1-CA123219-01A2, awarded by the National Institutes of Health, and DE-AC03-76SF00098, awarded by the Department of Energy. The Government has certain rights in the invention.