Abstract

Abstract Vulvar cancer is a rare but aggressive form of cancer that remains understudied. Our results show that treatment of the vulvar cancer cell line, UMSCV-4, with the glucocorticoid, clobetasol, increases apoptosis. Clobetasol is often used to treat a common inflammatory disease of the vulva known as vulvar lichen sclerosus (VLS) and up to 65% of vulvar carcinomas arise in the background of VLS. This would indicate clobetasol may also decrease the progression of vulvar cancer, if our observations reflect what is happening in vivo. However, our studies also show that apoptosis is not universal for the clobetasol treated UMSCV-4 cells. A subpopulation appears to enter a state of quiescence as evidenced by the return of some of the cells to normal cell proliferation upon removal of clobetasol. We previously showed that p27Kip1 is upregulated in the clobetasol treated cells. Cells that were incubated in clobetasol for three months and then removed from clobetasol (UMSCV-4 LT), allowing them to reenter the cell cycle, no longer expressed high levels of p27Kip1 upon re-exposure to clobetasol. We are now examining the differential phosphorylation states of p27Kip1 in the untreated and treated cells as well as identifying other genes important to clobetasol induced quiescence using RNAseq. Citation Format: Jani E. Lewis, Mack Ogden, Gianna Minnuto, Kia Haering, Luke North. Clobetasol differentially effects the vulvar cancer cell line, UMSCV-4, causing both increases in apoptosis while maintaining a subpopulation in quiescence [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 1641.

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