首页> 外文期刊>European review for medical and pharmacological sciences. >MicroRNA-144-3p inhibits cell proliferation and promotes apoptosis in castration-resistant prostate cancer by targeting CEP55
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MicroRNA-144-3p inhibits cell proliferation and promotes apoptosis in castration-resistant prostate cancer by targeting CEP55

机译:MicroRNA-144-3p通过靶向CEP55抑制去势抵抗性前列腺癌的细胞增殖并促进其凋亡

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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.
机译:目的:MicroRNA-144-3p(miR-144-3p)与多种癌症的发生有关。然而,其在去势抵抗性前列腺癌(CRPC)中的作用仍然未知。这项研究旨在探讨miR-144-3p在CRPC发展中的生物学作用。材料与方法:进行RT-qPCR检测miR-144-3p在CRPC组织中的表达水平。用miR-144-3p或NC转染CRPC细胞。使用MTT和集落形成测定法来确定细胞生长。流式细胞仪检测细胞凋亡。萤光素酶报告基因检测用于预测由miR-144-3p调控的靶基因。最后,将siCEP55或siNC转染到DU145细胞中,测定细胞增殖和凋亡率。蛋白表达水平通过蛋白质印迹分析确认。结果:与雄激素依赖性前列腺癌(ADPC)肿瘤相比,CRPC组织和细胞系中的MiR-144-3p表达均显着降低。 miR-144-3p在CRPC细胞中的过表达有效抑制了这些CRPC细胞的增殖和集落形成并促进了细胞凋亡。此外,miR-144-3p直接靶向中心体蛋白55(CEP55),并抑制CEP55表达。最后,CEP55沉默显着抑制CRPC细胞增殖并诱导其凋亡,表明miR-144-3p通过下调CEP55影响CRPC细胞存活和增殖。结论:MiR-144-3p通过直接靶向CEP55充当CRPC细胞的肿瘤抑制因子,而CEP55似乎是CRPC的新型治疗靶点。

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