Discipline: Biological Sciences
Subcategory: Cancer Research
Room: Exhibit Hall
Mojisoluwa Awolowo - Morgan State University
Co-Author(s): Taaliah Campbell, Morgan State University, Baltimore, Maryland; Ohoud Hawsawi, Clark Atlanta University, Atlanta, GA; Valerie Odero-Marah, Morgan State University, Baltimore, Maryland.
Prostate cancer (PCa) is the most common non-skin cancer in men, and second leading cause of death. PCa occurs when cells within the prostate grow uncontrollably, creating small tumors. Generally, the growth/proliferation of the prostate is regulated by the male hormone, androgen, that binds androgen receptor (AR), a nuclear receptor that functions as a transcription factor and regulates the development and proliferation of the prostate as well as PCa. High Mobility Group AT-Hook (HMGA2) is a transcription factor protein that alters the structure of DNA by binding to the promoter region to regulate the transcription of genes. The expression of HMGA2 is associated with cancer proliferation and metastasis and is higher in PCa patients compared to patients without cancer. Additionally, this gene has two isoforms HMGA2 full-length/wild-type and truncated (missing the carboxyl terminus). Preliminary studies show that AR is localized in the nucleus of HMGA2 wild-type but not truncated overexpressing cells. Our goal was to investigate whether HMGA2 wild-type promotes AR translocation to the nucleus which leads to increased cell proliferation in PCa cells. We utilized HMGA2-wild-type and HMGA2-truncated overexpressing LNCaP cells to knockdown either AR or HMGA2 with siRNA followed by western blot analysis, cell proliferation assay, and immunofluorescence. Our results show that HMGA2 siRNA led to decreased expression of wild-type (25 kDa long form) and truncated isoform (17 kDa) protein expression, and cell proliferation when compared to control siRNA. However, AR knockdown decreased AR expression in both cell lines but only decreased cell proliferation in HMGA2-wild-type cells. This suggests that HMGA2 wild-type works with AR to promote cell proliferation, whereas HMGA2-truncated promotes cell proliferation by an AR-independent mechanism. Therefore, we need to examine how current PCa treatments such as enzalutamide that target AR work in patients expressing differing HMGA2 isoforms.
Funder Acknowledgement(s): NIH RISE 5R25GM058904
Faculty Advisor: Valerie Odero-Marah, email@example.com
Role: I contributed to all parts of the experiment including but not limited to cell culture, western blotting, siRNA treatment, knockdown and proliferation assay.