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Androgen‐responsive tripartite motif 36 enhances tumor‐suppressive effect by regulating apoptosis‐related pathway in prostate cancer

机译:雄激素反应性三方基序36通过调节前列腺癌的凋亡相关途径来增强肿瘤抑制作用

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摘要

Tripartite motif 36 (TRIM36) belongs to the TRIM family, most members of which are involved in ubiquitination and degradation of target proteins by functioning as E3 ubiquitin ligases. The function of TRIM36 has not been well documented, therefore, we investigated the clinical significance and function of TRIM36 in human prostate cancer (PC). Multivariate logistic regression analysis showed that TRIM36 immunoreactivity was an independent predictor of cancer‐specific survival of PC patients. Gain‐of‐function study revealed that overexpression of TRIM36 suppressed cell proliferation and migration of LNCaP, 22Rv1, and DU145 cells. Moreover, TRIM36 knockdown using siRNA suppressed apoptosis and promoted cell proliferation and migration in LNCaP and 22Rv1 cells. Furthermore, our microarray analysis revealed that the apoptosis‐related pathway was significantly upregulated by TRIM36 overexpression. The TUNEL assay showed that apoptosis promoted by docetaxel treatment was alleviated in siTRIM36‐treated style="fixed-case">LNCaP and 22Rv1 cells. Taken together, these results suggest that high expression of style="fixed-case">TRIM36 is associated with favorable prognosis and that style="fixed-case">TRIM36 plays a tumor‐suppressive role by inhibiting cell proliferation and migration as well as promoting apoptosis in style="fixed-case">PC.
机译:三方基序36(TRIM36)属于TRIM家族,其大多数成员通过充当E3泛素连接酶参与靶蛋白的泛素化和降解。 TRIM36的功能尚未得到充分证明,因此,我们调查了TRIM36在人前列腺癌(PC)中的临床意义和功能。多元logistic回归分析表明,TRIM36免疫反应性是PC患者癌症特异性生存的独立预测因子。功能获得性研究表明,TRIM36的过表达抑制了LNCaP,22Rv1和DU145细胞的细胞增殖和迁移。此外,使用siRNA进行的TRIM36抑制可抑制LNCaP和22Rv1细胞的凋亡并促进细胞增殖和迁移。此外,我们的微阵列分析表明,TRIM36过表达显着上调了细胞凋亡相关途径。 TUNEL分析显示,经siTRIM36处理的 style =“ fixed-case”> LNC aP和22Rv1细胞,多西他赛治疗促进的细胞凋亡得到缓解。综上所述,这些结果表明 style =“ fixed-case”> TRIM 36的高表达与预后良好相关,并且 style =“ fixed-case”> TRIM 36发挥了作用通过抑制 style =“ fixed-case”> PC 中的细胞增殖和迁移以及促进细胞凋亡来抑制肿瘤。

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