B You1, K-C Zhang. 1. Department of Urology, Traditional Chinese Medicine Hospital of Taian, Taian, Shandong Province, China. zzz020609@163.com.
Abstract
OBJECTIVE: MicroRNA-144-3p (miR-144-3p) has been implicated in the tumorigenesis of multiple types of cancer. However, its role in castration-resistant prostate cancer (CRPC) remains largely unknown. This study aimed to explore the biological role of miR-144-3p in the development of CRPC. MATERIALS AND METHODS: RT-qPCR was performed to measure the expression levels of miR-144-3p in CRPC tissues. CRPC cells were transfected with miR-144-3p or NC. MTT and colony formation assays were used to determine cell growth; flow cytometry was used to measure apoptosis; a luciferase reporter assay was used to predict the target genes regulated by miR-144-3p. Finally, siCEP55 or siNC was transfected into DU145 cells, and the rates of cell proliferation and apoptosis were measured. Protein expression levels were confirmed by Western blot analysis. RESULTS: MiR-144-3p expression was significantly decreased in both CRPC tissues and cell lines compared with that from androgen-dependent prostate cancer (ADPC) tumors. Overexpression of miR-144-3p in CRPC cells effectively inhibited proliferation and colony formation and promoted apoptosis in these CRPC cells. Additionally, miR-144-3p directly targeted centrosomal protein 55 (CEP55) and suppressed CEP55 expression. Finally, CEP55 silencing remarkably suppressed proliferation and induced apoptosis of CRPC cells, indicating that miR-144-3p affects CRPC cell survival and proliferation by downregulating CEP55. CONCLUSIONS: MiR-144-3p serves as a tumor suppressor in CRPC cells by directly targeting CEP55, which appears to be a novel therapeutic target for CRPC.
OBJECTIVE: MicroRNA-144-3p (miR-144-3p) has been implicated in the tumorigenesis of multiple types of cancer. However, its role in castration-resistant prostate cancer (CRPC) remains largely unknown. This study aimed to explore the biological role of miR-144-3p in the development of CRPC. MATERIALS AND METHODS: RT-qPCR was performed to measure the expression levels of miR-144-3p in CRPC tissues. CRPC cells were transfected with miR-144-3p or NC. MTT and colony formation assays were used to determine cell growth; flow cytometry was used to measure apoptosis; a luciferase reporter assay was used to predict the target genes regulated by miR-144-3p. Finally, siCEP55 or siNC was transfected into DU145 cells, and the rates of cell proliferation and apoptosis were measured. Protein expression levels were confirmed by Western blot analysis. RESULTS: MiR-144-3p expression was significantly decreased in both CRPC tissues and cell lines compared with that from androgen-dependent prostate cancer (ADPC) tumors. Overexpression of miR-144-3p in CRPC cells effectively inhibited proliferation and colony formation and promoted apoptosis in these CRPC cells. Additionally, miR-144-3p directly targeted centrosomal protein 55 (CEP55) and suppressed CEP55 expression. Finally, CEP55 silencing remarkably suppressed proliferation and induced apoptosis of CRPC cells, indicating that miR-144-3p affects CRPC cell survival and proliferation by downregulating CEP55. CONCLUSIONS: MiR-144-3p serves as a tumor suppressor in CRPC cells by directly targeting CEP55, which appears to be a novel therapeutic target for CRPC.