Department of Radiotherapy, Jiangsu Province Danyang People's Hospital, Danyang, China.
Eur Rev Med Pharmacol Sci. 2018 Oct;22(20):6816-6823. doi: 10.26355/eurrev_201810_16149.
To detect the expression of microRNA-556-3p in esophageal cancer (EC) tissues and to elucidate the mechanisms underlying microRNA-556-3p in promoting EC progression.
QRT-PCR (quantitative Real-Time Polymerase Chain Reaction) was performed to detect microRNA-556-3p expression in 65 cases of EC tissues, 30 cases of normal esophageal tissues and EC cell lines. The overall survival (OS) of EC patients was calculated based on the 10-year follow-up data. For in vitro experiments, MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) and transwell assay were performed to evaluate the effect of microRNA-556-3p on the proliferative and invasive abilities of EC cells. The effect of microRNA-556-3p on DAB2IP and MAPK pathway was determined by Western blot and qRT-PCR. The binding condition between microRNA-556-3p and DAB2IP was further confirmed by Luciferase reporter gene assay.
MicroRNA-556-3p expression was upregulated in EC tissues than that of paracancerous tissues. EC patients with higher expression of microRNA-556-3p presented a shorter OS than those with lower expression. Moreover, microRNA-556-3p overexpression in EC cells remarkably promoted cell viability. Upregulated microRNA-556-3p in Eca109 and Eca7906 cell lines markedly increased cell proliferation and invasion. The expression level of DAB2IP was negatively regulated by microRNA-556-3p verified by the Luciferase reporter gene assay.
MicroRNA-556-3p blocked the translation of DAB2IP at mRNA level by directly binding to 3'UTR of DAB2IP, thereafter enhancing the proliferation of Eca109 and Eca7906 cells. MicroRNA-556-3p promoted the occurrence and development of EC. Our study provided a new theoretical basis and therapeutic target for EC treatment.
检测微小 RNA-556-3p 在食管癌（EC）组织中的表达，并阐明微小 RNA-556-3p 促进 EC 进展的机制。
采用实时定量聚合酶链反应（qRT-PCR）检测 65 例 EC 组织、30 例正常食管组织和 EC 细胞系中微小 RNA-556-3p 的表达。根据 10 年随访数据计算 EC 患者的总生存期（OS）。体外实验中，采用 MTT（3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴盐）和 Transwell 测定法评估微小 RNA-556-3p 对 EC 细胞增殖和侵袭能力的影响。采用 Western blot 和 qRT-PCR 确定微小 RNA-556-3p 对 DAB2IP 和 MAPK 通路的影响。通过荧光素酶报告基因测定进一步证实微小 RNA-556-3p 与 DAB2IP 的结合情况。
微小 RNA-556-3p 在 EC 组织中的表达高于癌旁组织。微小 RNA-556-3p 表达较高的 EC 患者 OS 较表达较低的患者短。此外，EC 细胞中微小 RNA-556-3p 的过表达显著促进了细胞活力。Eca109 和 Eca7906 细胞系中上调的微小 RNA-556-3p 明显增加了细胞增殖和侵袭。荧光素酶报告基因测定证实微小 RNA-556-3p 通过直接结合 DAB2IP 的 3'UTR 负调控 DAB2IP 的表达。
微小 RNA-556-3p 通过直接结合 DAB2IP 的 3'UTR 阻断 DAB2IP 的翻译，进而增强 Eca109 和 Eca7906 细胞的增殖。微小 RNA-556-3p 促进了 EC 的发生和发展。我们的研究为 EC 的治疗提供了新的理论基础和治疗靶点。
