Submission Type
Poster
Abstract
Quiescence is a reversible cellular state where a cell exits the cell cycle and ceases replication in response to stress. Cells can re-enter the cycle once the stress is alleviated. Emerging evidence suggests that cells in a quiescent state may contribute to the long-term dormancy of cancer cells. Vulvar squamous cell carcinoma (VSCC) is a rare form of female genital cancer, and while its treatment and diagnosis remain poorly understood, ultrapotent topical corticosteroids like clobetasol are commonly used to treat vulvar lichen sclerosus (VLS), a skin condition that can precede vulvar cancer development. Our studies show that a subpopulation of the vulvar cancer cell line, UMSCV-4, enters a state of quiescence upon clobetasol exposure. After removal of clobetasol, this subpopulation re-enters the cell cycle. Using BrdU incorporation, a measure of DNA synthesis, we quantified the clobetasol-induced decrease in proliferation and assessed how quickly cells re-enter the cycle post-treatment. Notably, many cells did not re-enter the cell cycle, prompting us to use a caspase-3 assay to determine if these cells were undergoing programmed cell death or apoptosis. Finally, we examined the expression of two proteins, p27 and p57, which are linked to quiescence induced by glucocorticoid receptor activation in lung cancer. Both proteins are tumor suppressors that regulate cell proliferation by inhibiting complexes that drive progression through the cell cycle. Since clobetasol acts through the glucocorticoid receptor, we measured the expression levels of these proteins using western blot analysis of cell extracts after clobetasol treatment.
Recommended Citation
Marsello, Claudia, "162 - Examining the Involvement of p27 and p57 in Clobetasol Induced Quiescence in the Vulvar Cancer Cell Line, UMSCV-4." (2025). GREAT Day Posters. 40.
https://knightscholar.geneseo.edu/great-day-symposium/great-day-2025/posters-2025/40
162 - Examining the Involvement of p27 and p57 in Clobetasol Induced Quiescence in the Vulvar Cancer Cell Line, UMSCV-4.
Quiescence is a reversible cellular state where a cell exits the cell cycle and ceases replication in response to stress. Cells can re-enter the cycle once the stress is alleviated. Emerging evidence suggests that cells in a quiescent state may contribute to the long-term dormancy of cancer cells. Vulvar squamous cell carcinoma (VSCC) is a rare form of female genital cancer, and while its treatment and diagnosis remain poorly understood, ultrapotent topical corticosteroids like clobetasol are commonly used to treat vulvar lichen sclerosus (VLS), a skin condition that can precede vulvar cancer development. Our studies show that a subpopulation of the vulvar cancer cell line, UMSCV-4, enters a state of quiescence upon clobetasol exposure. After removal of clobetasol, this subpopulation re-enters the cell cycle. Using BrdU incorporation, a measure of DNA synthesis, we quantified the clobetasol-induced decrease in proliferation and assessed how quickly cells re-enter the cycle post-treatment. Notably, many cells did not re-enter the cell cycle, prompting us to use a caspase-3 assay to determine if these cells were undergoing programmed cell death or apoptosis. Finally, we examined the expression of two proteins, p27 and p57, which are linked to quiescence induced by glucocorticoid receptor activation in lung cancer. Both proteins are tumor suppressors that regulate cell proliferation by inhibiting complexes that drive progression through the cell cycle. Since clobetasol acts through the glucocorticoid receptor, we measured the expression levels of these proteins using western blot analysis of cell extracts after clobetasol treatment.
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