Discipline: Biological Sciences
Subcategory: Cell and Molecular Biology
Session: 3
Room: Exhibit Hall A
Felicia White - Clark Atlanta University
Co-Author(s): Ana Cecilia Millena, John Davis and Shafiq Khan
Carcinogenesis. Our recent studies show that JunD is essential for cell proliferation in prostate (PCa) cancer cells, while other Jun family members play little, if any, role in induction of cell proliferation in these cells. We also demonstrated that specific knock-down (KD) of JunD in PCa cells resulted in cell cycle arrest in G1-phase concomitant with a decrease in the levels of Id1, c-MYC, and Ki67, but an increased in p21 protein levels. In this study, we investigated the role of JunD in ovarian cancer cell proliferation, focusing on SK0V3 and CA0V3 cell lines. Cells were cultured in recommended media as described previously. Small interfering RNAs for JunD were transfected in SK0V3 and CA0V3 cells to knockdown JunD expression. Cell growth assays were performed by manually counting the cells using Nexcelcom?s Cellometer Vision. Selective knockdown of JunD expression resulted in significant reduction in cell proliferation in SK0V3 cells but not in CA0V3. Interestingly, we observed that CA0V3 cell line has high level of basal c-MYC and PRDX3 which may suggest its resistance to exogenous JunD silencing. We plan to extend this study to additional ovarian cancer models to have a better understanding of JunD?s role in ovarian cancer cell proliferation.
Funder Acknowledgement(s): ACKNOWLEDGEMENT: These studies were supported by the NIH/NIMHD/RCMI grant#2G12RR003062 and NIH/NIMHD P20 grant #5P20MD002285
Faculty Advisor: Felicia White, skhan@cau.edu
Role: Western blots, migration assays, cell culture and cell quantification.