Submission Type
Poster
Abstract
Vulvar squamous cell carcinoma (VSSC) is a rare yet aggressive cancer, primarily affecting women over 60, with early stages often masked by vulvar lichen sclerosis (VLS). VLS is typically treated with ultrapotent corticosteroids like clobetasol. Our previous work showed that clobetasol treatment of A431 vulvar cancer cells leads to a loss of the cell-cell junction protein E-cadherin and a gain of the intermediate filament protein vimentin. These changes are associated with an epithelial-to-mesenchymal transition (EMT), a process linked to cancer progression and the acquisition of a more aggressive phenotype. Interestingly, A431D cells, derived from clobetasol-treated A431 cells, do not lose expression of the epithelial intermediate filaments, cytokeratins 8 and 18. This study explores the roles of vimentin, cytokeratins 8 and 18, and adherens junction components (E-cadherin and plakoglobin) in driving the morphology of these vulvar cancer cells. Using molecular and cellular biology techniques, including plasmid transfections and immunofluorescence microscopy, we introduce E-cadherin-plakoglobin constructs into A431D cells to assess their impact on the intermediate filament network. We hypothesized that E-cadherin-plakoglobin constructs, which reestablish adherens junctions and desmosomes, will restore a cytoarchitecture pattern typical of epithelial cells. In contrast, constructs lacking essential domains for adherens junction and desmosome formation will fail to alter the distribution of cytokeratins and vimentin. This study aims to deepen our understanding of cytoskeletal remodeling in cancer progression.
Recommended Citation
Gopal, Avinash; Mongelli, Sara; Stevenson, Abby; and Trojanowski, Trinity, "224 - Understanding the influence of different intermediate filaments on the morphology of the vulvar cancer cell line, A431D." (2025). GREAT Day Posters. 67.
https://knightscholar.geneseo.edu/great-day-symposium/great-day-2025/posters-2025/67
224 - Understanding the influence of different intermediate filaments on the morphology of the vulvar cancer cell line, A431D.
Vulvar squamous cell carcinoma (VSSC) is a rare yet aggressive cancer, primarily affecting women over 60, with early stages often masked by vulvar lichen sclerosis (VLS). VLS is typically treated with ultrapotent corticosteroids like clobetasol. Our previous work showed that clobetasol treatment of A431 vulvar cancer cells leads to a loss of the cell-cell junction protein E-cadherin and a gain of the intermediate filament protein vimentin. These changes are associated with an epithelial-to-mesenchymal transition (EMT), a process linked to cancer progression and the acquisition of a more aggressive phenotype. Interestingly, A431D cells, derived from clobetasol-treated A431 cells, do not lose expression of the epithelial intermediate filaments, cytokeratins 8 and 18. This study explores the roles of vimentin, cytokeratins 8 and 18, and adherens junction components (E-cadherin and plakoglobin) in driving the morphology of these vulvar cancer cells. Using molecular and cellular biology techniques, including plasmid transfections and immunofluorescence microscopy, we introduce E-cadherin-plakoglobin constructs into A431D cells to assess their impact on the intermediate filament network. We hypothesized that E-cadherin-plakoglobin constructs, which reestablish adherens junctions and desmosomes, will restore a cytoarchitecture pattern typical of epithelial cells. In contrast, constructs lacking essential domains for adherens junction and desmosome formation will fail to alter the distribution of cytokeratins and vimentin. This study aims to deepen our understanding of cytoskeletal remodeling in cancer progression.
Comments
Sponsored by Jani Lewis