The role of septin-2 in the progression of epithelial ovarian cancer.
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Ovarian cancer is the fifth leading cause of cancer mortality in women and the second most common gynecological cancer. Epithelial ovarian cancer, the most lethal and most common form, has a five-year survival rate of 47% and accounts for 95% of ovarian malignancies. Limited development of effective therapies has led to a stagnate overall survival rate and lack of options for patients undergoing treatments, leading many researchers to continue to search for possible therapeutic targets. The septin protein family is a highly conserved family of GTP-binding proteins that interact with the cellular membrane, provide scaffolding for protein attachments, and assist in cell migration. Septin-2 has recently been implicated in the tumorigenesis of epithelial ovarian cancer through altering cellular metabolism and other mechanisms. The objective of this investigation is to continue to study the role of septin-2 protein expression in the pathogenesis of epithelial ovarian cancer. We will investigate tumorigenic properties of cells that overexpress septin-2 and septin-2 knockdown cells. Thus far, successful completion of knockdown cell lines was performed in ES-2 and SKOV-3 cell lines, but overexpression cell lines were not as successful, as a significant increase in the septin-2 protein was not observed. WNT1 protein localization changed from the nucleus to the cytoplasm in the SKOV-3 cell line only when septin-2 was downregulated, indicative of a change in the WNT1 signaling pathway in those cells. Furthermore, SKOV-3 knockdown septin-2 cells form less tightly compact spheroids than control SKOV-3 cells. This study may provide insights into septin-2 as a possible target for treatment.
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