Small cell carcinoma of the ovary, hypercalcemic type (SCCOHT), is a rare and aggressive cancer with limited treatment options. The cancer is driven by the loss of the SWI/SNF chromatin remodeling complex subunit member, BRG1. It is hypothesized that this loss of BRG1 creates a dependency on the additional SWI/SNF subunits that remain expressed. This study aims to investigate the role of one of these retained SWI/SNF subunits, called SNF5, in promoting the expression of genes that may be linked to cancer. To study SNF5, the SCCOHT cell line, COV-434 was engineered using CRISPR-Cas9 technology to remove endogenous expression of SNF5 and replace it with a version of SNF5 that can be induced exogenously using a small chemical called doxycycline. The goals of this project are two-fold: 1) validate the COV-434 cell line and confirm the controlled expression of SNF5 and 2) determine genes regulated by SNF5. Preliminary results indicate that 1 µg/ml doxycycline successfully induces SNF5 expression and that SNF5 regulates a variety of genes linked to known cancer processes. These results set a foundation for understanding the role of SNF5 in SCCOHT cell line function and may provide valuable insight into how retained SWI/SNF complexes function in other cancers driven by loss of SWI/SNF subunits.
Investigating the effect of SNF5 on cell lines derived from small cell carcinoma of the ovary, hypercalcemic type cancers
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Student Abstract Submission