This study aims to investigate the expression of retinoblastoma binding protein 6 (RBBP6) in prostate cancer (PCa) and its association with the c‐Jun N‐terminal kinase (JNK) pathway. Immunohistochemistry was used to detect RBBP6 and JNK1/2 expression in PCa and benign prostatic hyperplasia tissues. RBBP6 expression in PCa cells (LNCap, PC3, and DU145) and noncancerous prostate epithelial cells (RWPE‐1) was determined by quantitative real‐time polymerase chain reaction and western blot analysis. PC3 and DU145 cells were transfected with RBBP6 small interfering RNAs (siRNAs) to examine the biological characteristics. Anisomycin (a JNK activator) with/without RBBP6 siRNA was used to treat PC3 cells for further investigating the ramification of the RBBP6‐mediated JNK pathway in PCa. PCa tissues and cells showed higher RBBP6 and JNK1/2 expression. RBBP6 was positively correlated with JNK1/2 in PCa tissues. Besides, RBBP6 expression was correlated to clinical tumor stage, lymph node metastasis, Gleason grade, preoperative prostate‐specific antigen level, as well as prognosis of PCa. RBBP6 siRNA reduced cell proliferation, arrested cells at G2/M, and promoted cell apoptosis, and suppressed JNK pathway. In addition, migration and invasion decreased after the RBBP6 siRNA transfection with downregulated matrix metallopeptidase‐2 (MMP‐2) and MMP‐9. Anisomycin promoted the proliferation, invasion, and migration of PC3 cells and inhibited PC3 cell apoptosis, which could be reversed by RBBP6 siRNA. RBBP6 expression was upregulated in PCa tissues and positively correlated with expression level of JNK1/2. With inhibition of RBBP6 expression, the proliferation, invasion, and migration of PCa cells decreased dramatically, while PC3 cell apoptosis increased appreciably, accompanied by the suppression of the JNK pathway.

中文翻译：

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分析视网膜母细胞瘤结合蛋白 6 与前列腺癌中 JNK 信号通路的表达和关联。

本研究旨在研究视网膜母细胞瘤结合蛋白 6 (RBBP6) 在前列腺癌 (PCa) 中的表达及其与 c-Jun N 末端激酶 (JNK) 通路的关联。免疫组化用于检测PCa和良性前列腺增生组织中RBBP6和JNK1/2的表达。RBBP6 在 PCa 细胞（LNCap、PC3 和 DU145）和非癌性前列腺上皮细胞 (RWPE-1) 中的表达通过定量实时聚合酶链反应和蛋白质印迹分析确定。用 RBBP6 小干扰 RNA (siRNA) 转染 PC3 和 DU145 细胞以检查生物学特性。有/没有 RBBP6 siRNA 的茴香霉素（一种 JNK 激活剂）用于处理 PC3 细胞，以进一步研究 RBBP6 介导的 JNK 通路在 PCa 中的分支。PCa 组织和细胞显示出更高的 RBBP6 和 JNK1/2 表达。RBBP6 与 PCa 组织中的 JNK1/2 呈正相关。此外，RBBP6的表达与临床肿瘤分期、淋巴结转移、Gleason分级、术前前列腺特异性抗原水平以及PCa预后相关。RBBP6 siRNA减少细胞增殖，将细胞阻滞在G2/M，促进细胞凋亡，抑制JNK通路。此外，RBBP6 siRNA 转染下调的基质金属肽酶-2 后，迁移和侵袭减少。MMP-2 ) 和MMP-9。茴香霉素促进PC3细胞增殖、侵袭和迁移，抑制PC3细胞凋亡，RBBP6 siRNA可以逆转这种作用。RBBP6 表达在 PCa 组织中上调，并与 JNK1/2 的表达水平呈正相关。随着RBBP6表达的抑制，PCa细胞的增殖、侵袭和迁移显着减少，而PC3细胞凋亡明显增加，伴随着JNK通路的抑制。