Presenter Information

Kia Haering, SUNY GeneseoFollow

Submission Type

Poster

Start Date

4-26-2023

Abstract

As epithelial carcinomas progress to a malignant state, the expression of tissue-specific genes is altered. In the case of vulvar epithelial carcinoma cell line A431, the tumor suppressor gene E-cadherin is expressed, as well as cytokeratins 8 and 18. E-cadherin is an integral membrane protein that facilitates cellular adhesion. Cytokeratins 8 and 18 are intermediate filaments located on the cytoplasmic side of the plasma membrane and help resist mechanical stress. Clobetasol is a glucocorticoid that is used to treat vulvar lichen sclerosus, an inflammatory condition that predisposes patients to the development of vulvar carcinomas. When the cell line A431 is treated with clobetasol, the resulting cells lose expression of E-cadherin and partial expression of cytokeratins 8 and 18, while gaining expression of vimentin. Vimentin is an intermediate filament bound to intracellular integrins and the extracellular matrix of the cell which provides structural support. The change in tissue-specific gene expression is indicative of an epithelial-mesenchymal transition, wherein cancer cells become more aggressive and may invade other tissues. Immunofluorescence was used to identify the changes in gene expression. Raman Spectroscopy has been used in an attempt to visualize the surface proteins of untreated and treated cells as the transition advances toward a malignant state. In observing the cellular reconstruction of the epithelial-presenting A431 to clobetasol-treated A431D cells as a function of time, the regulation of gene expression and interactions of co-expressed genes can be used to isolate the epigenetic mechanism involved in the epithelial-mesenchymal transition of cell line A431.

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Sponsored by Kazushige Yokoyama, Jani Lewis

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Apr 26th, 12:00 AM

265 - Visualizing Altered Gene Expression of Clobetasol Treated Vulvar Carcinoma Cells with Raman Spectroscopy

As epithelial carcinomas progress to a malignant state, the expression of tissue-specific genes is altered. In the case of vulvar epithelial carcinoma cell line A431, the tumor suppressor gene E-cadherin is expressed, as well as cytokeratins 8 and 18. E-cadherin is an integral membrane protein that facilitates cellular adhesion. Cytokeratins 8 and 18 are intermediate filaments located on the cytoplasmic side of the plasma membrane and help resist mechanical stress. Clobetasol is a glucocorticoid that is used to treat vulvar lichen sclerosus, an inflammatory condition that predisposes patients to the development of vulvar carcinomas. When the cell line A431 is treated with clobetasol, the resulting cells lose expression of E-cadherin and partial expression of cytokeratins 8 and 18, while gaining expression of vimentin. Vimentin is an intermediate filament bound to intracellular integrins and the extracellular matrix of the cell which provides structural support. The change in tissue-specific gene expression is indicative of an epithelial-mesenchymal transition, wherein cancer cells become more aggressive and may invade other tissues. Immunofluorescence was used to identify the changes in gene expression. Raman Spectroscopy has been used in an attempt to visualize the surface proteins of untreated and treated cells as the transition advances toward a malignant state. In observing the cellular reconstruction of the epithelial-presenting A431 to clobetasol-treated A431D cells as a function of time, the regulation of gene expression and interactions of co-expressed genes can be used to isolate the epigenetic mechanism involved in the epithelial-mesenchymal transition of cell line A431.

 

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