Presentation Title

Analyzing the Role of MDMX in Regulating Cell Cycle Progression and Angiogenesis in Prostate Cancer cells

Presenter(s)

Ahmed AlsarraniFollow

Presenter Credentials

Ahmed Alsarrani, College of Pharmacy, fourth year, Ph.D.

Presenter Degree

Ph.D.

Co-Author Credentials

Thiagarajan Venkatesan, Ph.D., Associate Research Scientist, Rumbaugh-Goodwin Institute for Cancer Research, College of Pharmacy, Nova Southeastern University Umamaheswari Natarajan, Ph.D., Research Associate, Rumbaugh-Goodwin Institute for Cancer Research, College of Pharmacy, Nova Southeastern University Appu Rathinavelu, Ph.D., Professor, Rumbaugh-Goodwin Institute for Cancer Research, College of Pharmacy, Nova Southeastern University

College

College of Pharmacy

Campus Location

Ft. Lauderdale

Format

Poster

IRB Approval Verification

N/A

Abstract

Objective. The study was conducted to assess the p53-dependent and -independent effects of the proto-oncogene MDMX in regulating major proteins of cell cycle and angiogenesis in prostate cancer (PCa). Background. PCa is the second leading cause of cancer death in the USA. The five-year survival rate of distant stages of prostate cancer is low. MDMX and MDM2 are p53 regulators that are overexpressed in PCa cancer. Our previous study revealed that angiogenic genes were elevated in LNCaP-MST (MDM2 transfected cells) compared to LNCaP. The goal of our study is to understand the effect of MDMX and MDM2, in prostate cancer cells to determine how it regulates cancer growth and metastasis. Methods. In our study, the cell viability of prostate cancer cell cells (LNCaP) was measured using Trypan blue dye exclusion method after 24, and 48 h of NSC 207895 (NSC) and SJ-172550 (SJ-17) treatment. Also, western blot experiments were conducted to analyze the p21, VEGF, and MDM2 protein expression levels. Results. A significant reduction in VEGF expression was detected after treatment with both MDMX inhibitors. Interestingly, an elevating in p21 level was observed with NSC and SJ-17 treatments. Moreover, SJ-17 reduced the cell viability after 24, 48 h treatment in LNCaP cells. Conclusion. Our study showed that the MDMX overexpression could play a significant role in the angiogenesis process of prostate cancer. MDMX inhibition reduced angiogenesis through lowering VEGF levels and induced cell cycle arrest through p21 elevation. Grant. This research was funded by the Royal Dames of Cancer Research Inc., Florida.

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Analyzing the Role of MDMX in Regulating Cell Cycle Progression and Angiogenesis in Prostate Cancer cells

Objective. The study was conducted to assess the p53-dependent and -independent effects of the proto-oncogene MDMX in regulating major proteins of cell cycle and angiogenesis in prostate cancer (PCa). Background. PCa is the second leading cause of cancer death in the USA. The five-year survival rate of distant stages of prostate cancer is low. MDMX and MDM2 are p53 regulators that are overexpressed in PCa cancer. Our previous study revealed that angiogenic genes were elevated in LNCaP-MST (MDM2 transfected cells) compared to LNCaP. The goal of our study is to understand the effect of MDMX and MDM2, in prostate cancer cells to determine how it regulates cancer growth and metastasis. Methods. In our study, the cell viability of prostate cancer cell cells (LNCaP) was measured using Trypan blue dye exclusion method after 24, and 48 h of NSC 207895 (NSC) and SJ-172550 (SJ-17) treatment. Also, western blot experiments were conducted to analyze the p21, VEGF, and MDM2 protein expression levels. Results. A significant reduction in VEGF expression was detected after treatment with both MDMX inhibitors. Interestingly, an elevating in p21 level was observed with NSC and SJ-17 treatments. Moreover, SJ-17 reduced the cell viability after 24, 48 h treatment in LNCaP cells. Conclusion. Our study showed that the MDMX overexpression could play a significant role in the angiogenesis process of prostate cancer. MDMX inhibition reduced angiogenesis through lowering VEGF levels and induced cell cycle arrest through p21 elevation. Grant. This research was funded by the Royal Dames of Cancer Research Inc., Florida.