Investigating the Mechanism of microRNA on Prostate Cancer and its Effect Towards Androgen Receptor

Abstract

Prostate cancer (PC) is the second most common malignancy among men, with advanced stages often developing into castration-resistant prostate cancer (CRPC). This study investigates the role of microRNA-X in drug resistance and tumorigenesis by modulating androgen receptor (AR) signaling. microRNA-X exhibits dual functionality in cancer, acting as either a tumor suppressor or oncogene. The experimental approach utilized PC cell lines with differing AR expressions, including androgen-dependent and independent lines. Lentiviral transduction was employed to overexpress microRNA-X, followed by functional assays including MTT assays for drug sensitivity and RT-qPCR for gene expression analysis. Key findings indicated challenges in the overexpression of microRNA-X, attributed to complexities in lentiviral transduction and cellular compensatory mechanisms. While successful transduction was limited, the study underscores the potential regulatory role of microRNA-X in AR signaling and drug resistance pathways, suggesting its value as a therapeutic target in CRPC. This research contributes to understanding microRNA-X's impact on treatment outcomes and supports the development of novel strategies to combat CRPC.