Abstract 1441: p27Kip1 is upregulated in UMSCV-4 cells corresponding to entering a state of quiescence when treated with clobetasol

Abstract

Abstract Quiescence, the temporary exit from the cell cycle, presents therapeutic challenges to cancer management since it allows evasion of chemotherapy and radiotherapy treatment. Essential to the study of quiescence in carcinogenesis is an established model system. Our studies have found that clobetasol treatment of the vulvar cancer cell line, UMSCV-4 causes these cells to enter a state of dormancy. Subsequent removal of the cells from clobetasol show a return to normal cell proliferation, even after dormancy for 3 months. p27Kip1 protein has been used as marker for entry into quiescence. Using both antibodies against p27Kip1 and transfection of a modified p27Kip1 containing plasmid into the UMSCV-4 cells we found that p27Kip1 is upregulated by addition of clobetasol, reflecting that quiescence is being activated in the treated UMSCV-4 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 p27Kip1 upon re-exposure to clobetasol. This establishes the UMSCV-4 cells as a good model system for the study of clobetasol induced quiescence in vulvar squamous epithelial cells. The importance of this work is underscored by the observation that 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. Citation Format: Gianna Minnuto, Luke North, Mack Ogden, Kia Haering, Jani E. Lewis. p27Kip1 is upregulated in UMSCV-4 cells corresponding to entering a state of quiescence when treated with clobetasol [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 1441.