摘要
目的:探究miR-590-3p在甲状腺乳头状癌进展中的作用。方法:利用RT-PCR检测甲状腺乳头状癌患者标本及其细胞系中miR-590-3p的表达。利用CCK-8、EdU、划痕、Transwell实验以及细胞流式技术检测miR-590-3p对细胞相关功能的影响。Western blot检测上皮细胞-间充质转化(epithelial-mesenchymal transition,EMT)途径相关蛋白表达量的变化。结果:在甲状腺乳头状癌组织及细胞系中miR-590-3p的表达量明显低于癌旁组织和正常甲状腺滤泡上皮细胞。与对照组相比,干扰miR-590-3p明显提升TPC-1细胞的增殖活性(P <0.01),过表达miR-590-3p则降低K-1细胞的增殖活性(P <0.01)。干扰miR-590-3p可增加TPC-1细胞的迁移与侵袭能力,抑制细胞凋亡(P <0.01),过表达miR-590-3p则降低K-1细胞的迁移与侵袭能力,促进细胞凋亡(P <0.01)。同时可以抑制EMT相关蛋白的表达。结论:miR-590-3p在甲状腺乳头状癌的发生发展中发挥抑癌基因的作用,可能为甲状腺乳头状癌的治疗提供帮助。
Objective:This study aims to explore the function of miR-590-3 p in papillary thyroid cancer(PTC).Methods:We examined the miR-590-3 p expression in human PTC tissues and cell lines by RT-PCR.CCK-8,EdU,wound healing,Transwell,flow cytometry were performed to analyze PTC cell function.Changes of epithelial-mesenchymal transition(EMT)signaling proteins were detected by Western blot.Results:The expression of miR-590-3 p was decreased in PTC tissues and cell lines.Compared with the normal control,knockdown of miR-590-3 p promoted cell proliferation,migration,invasion and inhibited cell apoptosis in PTC cells(P<0.01).However,overexpression of miR-590-3 p inhibited cell proliferation,migration,invasion and promoted cell apoptosis in PTC cells(P<0.01).And miR-590-3 p significantly inhibited EMT process.Conclusion:MiR-590-3 p acts as a tumor suppressor in PTC carcinogenesis and metastasis,and may be a therapeutic target for PTC.
作者
童厚超
斯岩
张浩
蔡晶昇
沈美萍
Tong Houchao;Si Yan;Zhang Hao;Cai Jingsheng;Shen Meiping(Department of General Surgery,the First Affiliated Hospital of Nanjing Medical University,Nanjing 210029,China)
出处
《南京医科大学学报（自然科学版）》
CAS
CSCD
北大核心
2019年第6期873-879,共7页
Journal of Nanjing Medical University(Natural Sciences)
基金
江苏省卫生厅科研基金面上项目(H201203)
南京医科大学第一附属医院科技招标项目(20180513)
