Hu S-H, Zhao M-J, Wang W-X, Xu C-W, Wang G-D
Department of Clinical Laboratory, Affiliated Hospital of Dali University, Dali, China.
Clinical research center of Occupational disease, Shanghai Pulmonary Hospital,Tongji University School of Medicine, Shanghai, China.
Cell Mol Biol (Noisy-le-grand). 2017 May 20;63(5):68-74. doi: 10.14715/cmb/2017.63.5.13.
Renal cell carcinoma (RCC) is the most common renal neoplasms and metastatic is common. Previous data have shown that the tripartite motif (TRIM) family proteinswere implicated in human tumoriogenesis. In this study, we aimed to investigate the role of TRIM59 in the cell growth and migration in RCC. The expression of TRIM59 in human RCC tissues was initially examined by qRT-PCR. Alentivirus-based shRNA against TRIM59 (Lv-shTRIM59) was constructed. The effects of TRIM59 knockdown on cell proliferation were examined by in vitro MTT assay, colony formation assay and in vivo a mouse xenograft model of RCC. Cell migration and invasion after knockdown of TRIM59 were also examined by transwell assay. Our data showed that the mRNA level of TRIM59 in cancerous tissues was 2-fold increased as compared with non-cancerous tissues. Knockdown of TRIM59 in a RCC cell line 786-O significantly slowed down cell proliferative rate and decreased both the colony number and sizes. In the mouse model, knockdown of TRIM59 consistently inhibited tumor growth in vivo. Moreover, it was shown that cell migration and invasion were suppressed by 68% and 50%, respectively in TRIM59-depleted 786-O cells. Our data suggest that TRIM59 may serve as a pro-oncogenic protein in promoting the progression of RCC. Knockdown of TRIM59 may be a promising strategy concerning the early detection and treatment of RCC.
肾细胞癌（RCC）是最常见的肾脏肿瘤，且转移常见。既往数据表明，三联基序（TRIM）家族蛋白与人类肿瘤发生有关。在本研究中，我们旨在探讨TRIM59在RCC细胞生长和迁移中的作用。首先通过qRT-PCR检测TRIM59在人RCC组织中的表达。构建了基于慢病毒的针对TRIM59的短发夹RNA（Lv-shTRIM59）。通过体外MTT试验、集落形成试验以及体内RCC小鼠异种移植模型检测TRIM59敲低对细胞增殖的影响。通过Transwell试验检测TRIM59敲低后细胞的迁移和侵袭情况。我们的数据显示，癌组织中TRIM59的mRNA水平比癌旁组织增加了2倍。在RCC细胞系786-O中敲低TRIM59显著减慢了细胞增殖速率，并减少了集落数量和大小。在小鼠模型中，敲低TRIM59持续抑制体内肿瘤生长。此外，结果表明，在TRIM59缺失的786-O细胞中，细胞迁移和侵袭分别被抑制了68%和50%。我们的数据表明，TRIM59可能作为一种促癌蛋白促进RCC的进展。敲低TRIM59可能是RCC早期检测和治疗的一种有前景的策略。
