Advertisement
You are prohibited from using or uploading content you accessed through this website into external applications, bots, software, or websites, including those using artificial intelligence technologies and infrastructure, including deep learning, machine learning and large language models and generative AI.
Advertisement
You have accessJournal of UrologyProstate Cancer: Basic Research & Pathophysiology II1 Apr 2018

MP64-08 A NOVEL BIGUANIDE DERIVATIVE DRUG, IM176, INHIBITS PROSTATE CANCER

    View All Author Information

    INTRODUCTION AND OBJECTIVES

    Biguanides were originally developed for the treatment of hyperglycemia and type 2 diabetes mellitus. Recently, the biguanides metformin and phenformin have been shown to exert potential anticancer effects in prostate cancer. We evaluated the anti-cancer efficacy and mechanism of IM176, a novel biguanide derivate drug on prostate cancer using prostate cancer cell lines and patient-derived castration-resistant prostate cancer cell lines.

    METHODS

    Cell viability assay, annexin V-FITC apoptosis detection, microscopy with immunofluorescence staining, real-time quantitative reverse transcription-polymerase chain reaction, and western blotting were conducted. Efficacy of IM176 was also evaluated using 2 cell lines derived from castration-resistant prostate cancer patient.

    RESULTS

    IM176 dose-dependently inhibited cell viability in all prostate cancer cell lines at lowest IC50 concentrations (LNCaP: 18.5μM, 22Rv1: 36.8 μM) compared to those of metformin, and phenformin. IM176-mediated AMPK activation caused mTOR inhibition, and a decrement in the phosphorylation of p70S6K1 and S6. IM176 inhibited the expression of AR, AR-splice variant 7 (AR-V7) and prostate-specific antigen in LNCaP and 22Rv1. IM176 induced apoptosis with increased levels of cleavage of caspase-3, and annexin V-positive / PI-positive, respectively. Moreover, IM176 inhibited cell viability at lowest IC50 concentrations in 2 cell lines derived from castration-resistant prostate cancer patient. We evaluate the relationship between AMPK-mTOR pathway and AR signaling pathway by blocking each pathway separately. After AR knockdown, phosphorylation of AMPK was significantly increased. However, AR and AR-V7 were not increased after treating AMPK inhibitor, Compound C.

    CONCLUSIONS

    IM176 showed comparable anti-tumor effects via AMPK-mTOR pathway and AR signaling pathway with the lowest IC50 compared to other biguanide derivative drugs in prostate cancer cell lines, including patient-derived castration resistant prostate cancer cell line and may be a novel anti-cancer drug for the treatment of prostate cancer.