Abstract 4642: Quercetin inhibits prostate cancer by modulating molecules involved in apoptosis and cell proliferation

Abstract

Prostate cancer (PCa) remains the second leading cause of death in men, despite the multimodal options offered in the clinics. Long latency and indolent nature of PCa provides window of opportunity for preventive interventions using natural and synthetic agents. Quercetin, a bioflavonoid abundant in fruits and vegetables, has been reported to inhibit growth in cancer and reduce inflammation in conditions like prostatitis. Considering this, we investigated the chemo-preventive effects of Quercetin on PCa. The effects of Quercetin on apoptosis and associated proteins on both RNA and protein levels were determined using apoptosis assay, real-time qPCR and western blot, respectively. Furthermore, an antibody microarray was performed to observe changes induced by Quercetin on signaling molecules and possible mechanism of cell survival/apoptosis in PCa. PCa cells treated with Quercetin showed decreased cell proliferation in a time and dose dependent manner, while no significant effect was seen on normal prostate cells. Quercetin treatment also significantly induced apoptosis in PCa cells, as compared with untreated controls. Different phosphorylation status of key molecules (Bcl-2, Akt-1 and NF-k B) was observed following Quercetin treatment in PCa cell lines, as compared with untreated controls, which are known to be involved in supporting PCa progression. These results suggest that Quercetin could be a potential chemo-preventative agent capable of slowing down the progression of PCa, by increasing apoptosis and decreasing cell proliferation.

Note: This abstract was not presented at the meeting.

Citation Format: Ashely B. Ward, Hina Mir, Neeraj Kapur, Shailesh Singh. Quercetin inhibits prostate cancer by modulating molecules involved in apoptosis and cell proliferation. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 4642. doi:10.1158/1538-7445.AM2015-4642