He Wei, Feng Jianfang, Zhang Yan, Wang Yuanyuan, Zang Wenqiao, Zhao Guoqiang
Department of Oncology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Experimental Teaching Center of Medical Functional Science, Medical College of Henan University of Science and Technology, Luoyang, China.
Lab Invest. 2016 Mar;96(3):317-24. doi: 10.1038/labinvest.2015.134. Epub 2015 Nov 16.
miR-186 has been demonstrated to have a significant role as a tumor suppressor in many types of cancers. Nevertheless, its biological function in esophageal squamous cell carcinoma (ESCC) remains unknown. In the present study, we found that the expression level of miR-186 was downregulated in ESCC in comparison with the adjacent normal tissues and was significantly associated with differentiation level, TNM stage, and lymph node metastasis of ESCC. Functional experiments revealed that enforced overexpression of miR-186 in ESCC cells suppressed the proliferation, invasion, and induced the apoptosis of cells. Luciferase reporter assay and western blotting analysis were performed to verify the target gene regulated by miR-186, SKP2. Our findings established that the miR-186 has a suppressive role in ESCC progression via SKP2-mediated pathway, and this implies that miR-186 could be a potential therapeutic target for ESCC.
miR-186已被证明在多种癌症中作为肿瘤抑制因子发挥重要作用。然而，其在食管鳞状细胞癌（ESCC）中的生物学功能仍不清楚。在本研究中，我们发现与相邻正常组织相比，ESCC中miR-186的表达水平下调，并且与ESCC的分化程度、TNM分期和淋巴结转移显著相关。功能实验表明，在ESCC细胞中强制过表达miR-186可抑制细胞增殖、侵袭并诱导细胞凋亡。进行荧光素酶报告基因检测和蛋白质印迹分析以验证miR-186调控的靶基因SKP2。我们的研究结果表明，miR-186通过SKP2介导的途径在ESCC进展中起抑制作用，这意味着miR-186可能是ESCC的潜在治疗靶点。
