微小RNA-205通过激活AKT信号通路促进鼻咽癌细胞的增殖、迁移和侵袭。
MiR-205 promotes proliferation, migration and invasion of nasopharyngeal carcinoma cells by activation of AKT signalling.
作者信息
Mao Yanjiao, Wu Shixiu, Zhao Ruping, Deng Qinghua
机构信息
Department of Radiation Oncology, Hangzhou Cancer Hospital, Hangzhou First People's Hospital, Hangzhou, China.
Department of Radiation Oncology, Hangzhou Cancer Hospital, Hangzhou First People's Hospital, Hangzhou, China
出版信息
J Int Med Res. 2016 Apr;44(2):231-40. doi: 10.1177/0300060515576556. Epub 2016 Feb 15.
OBJECTIVE
To examine the role of microRNA (miR)-205 in proliferation, migration and invasion of nasopharyngeal carcinoma (NPC).
METHODS
The human NPC cell line CNE2 was transfected with miR-205 mimic, anti-miR-205 inhibitor or scrambled oligonucleotide (control). Cell proliferation was assessed via MTT assay. Cell migration and invasion were evaluated by transwell migration and Matrigel® invasion assay, respectively. Radiation induced apoptosis was quantified via Caspase-Glo3/7 assay. Apoptotic proteins and epithelial-mesenchymal transition (EMT) proteins were semiquantified by Western blot analysis.
RESULTS
Overexpression of miR-205 increased the proliferation, migration and invasion of CNE2 cells, and decreased radiation-induced apoptosis compared with control cells. MiR-205 overexpression downregulated E-cadherin and upregulated Snail expression via downregulation of PTEN and upregulation of AKT.
CONCLUSION
MiR-205 plays vital roles in tumourigenesis and tumour progression in NPC, and may be a potential treatment target.
目的
探讨微小RNA（miR）-205在鼻咽癌（NPC）增殖、迁移和侵袭中的作用。
方法
将miR-205模拟物、抗miR-205抑制剂或乱序寡核苷酸（对照）转染到人NPC细胞系CNE2中。通过MTT法评估细胞增殖。分别通过Transwell迁移实验和基质胶侵袭实验评估细胞迁移和侵袭。通过Caspase-Glo3/7法对辐射诱导的细胞凋亡进行定量。通过蛋白质免疫印迹分析对凋亡蛋白和上皮-间质转化（EMT）蛋白进行半定量分析。
结果
与对照细胞相比，miR-205过表达增加了CNE2细胞的增殖、迁移和侵袭，并降低了辐射诱导的细胞凋亡。miR-205过表达通过下调PTEN和上调AKT，下调E-钙黏蛋白并上调Snail表达。
结论
miR-205在NPC的肿瘤发生和肿瘤进展中起重要作用，可能是一个潜在的治疗靶点。
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