Submission Type
Poster
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 happeningin 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 p27Kip1is 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 p27Kip1upon re-exposure to clobetasol. We are now examining the differential phosphorylation states of p27Kip1in the untreated and treated cells as well as identifying other genes important to clobetasol induced quiescence using RNAseq.
Recommended Citation
Ogden, Mack, "152-Clobetasol Differentially Affects the Vulvar Cancer Cell Line, UMSCV-4, Causing Both Increases in Apoptosis while Maintaining a Subpopulation in Quiescence" (2024). GREAT Day Posters. 39.
https://knightscholar.geneseo.edu/great-day-symposium/great-day-2024/posters-2024/39
152-Clobetasol Differentially Affects the Vulvar Cancer Cell Line, UMSCV-4, Causing Both Increases in Apoptosis while Maintaining a Subpopulation in Quiescence
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 happeningin 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 p27Kip1is 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 p27Kip1upon re-exposure to clobetasol. We are now examining the differential phosphorylation states of p27Kip1in the untreated and treated cells as well as identifying other genes important to clobetasol induced quiescence using RNAseq.