Abstract

Abstract Prostate cancer (PC) management lacks any targeted therapies. Statins have shown anticancer effects against PC in both in vitro and in vivo studies. CX3CR1 is a receptor expressed by many cancer cells, including PC. In this research, we studies the interaction between atorvastatin and CX3CR1/fractalkine on androgen-dependent PC cell line 22Rv1 vs. normal prostatic cells, RWPE1. Experimental settings were based on testing effect of atorvastatin in presence of fractalkine or by removing its effect using fractalkine neutralizing antibodies. MTT proliferation assay and adhesion assay, together with testing the expression of CX3CR1, p-AKT and p-GSK-3 were used. Results showed that fractalkine partially blunts the effect atorvastatin on proliferation and adhesion of PC cells. Similar effects were not noticed on normal prostatic cells. Western blotting showed a dose-dependent reduction in the expression of CX3CR1, p-akt and p-GSK-3 in presence of fractalkine, that was further enhanced when fractalkine was neutralized using specific antibodies. Results suggest the deprivation of fractalkine as a synergistic mechanism to enhance effects of atorvastatin and probably other anticancer agents. Citation Format: Belal Al-Husein. Interaction of atorvastatin and CX3CR1-fractalkine in androgen-dependent prostate cancer cells: Effect on PI3K pathway [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 1979.

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