...
首页> 外文期刊>European review for medical and pharmacological sciences. >MIR22HG inhibits cell growth, migration and invasion through regulating the miR-24-3p/p27kip1 axis in thyroid papillary carcinomas
【24h】

MIR22HG inhibits cell growth, migration and invasion through regulating the miR-24-3p/p27kip1 axis in thyroid papillary carcinomas

机译:MIR22HG通过调节miR-24-3p / p27kip1轴抑制甲状腺乳头状癌的细胞生长,迁移和侵袭

获取原文

摘要

OBJECTIVE: To explore the underlying mechanism of ncRNA (MIR22HG) in thyroid papillary carcinomas. PATIENTS AND METHODS: 40 pairs of thyroid papillary carcinomas tissues and adjacent normal tissues were collected from patients of the First Affiliated Hospital of Guangxi Medical University, who underwent oral surgery. qRT-PCR was applied to detect the expression of MIR22HG, miR-24-3p and p27kip1 in tissues and cells. Western blot was used to measure the protein level of p27kip1 in tissues and cells. Kaplan-Meier plot was used to analyze the overall survival rates in thyroid papillary carcinomas. Pearson’s correlation analysis was used to analyze the correlation relationship among MIR22HG, miR-24-3p and p27kip1 expression. Flow cytometric assay was applied to measure cell apoptosis. Transwell assay was used to assess cell migration and invasion abilities. Luciferase reporter assay was applied to verify the molecular relationships among MIR22HG, miR-24-3p and p27kip1 in thyroid papillary carcinomas. RESULTS: LncRNA MIR22HG and p27kip expressed low while miR-24-3p expressed high in thyroid papillary carcinomas and cells. Overexpression of MIR22HG inhibited cell proliferation, migration and invasion, whereas promoted cell apoptosis in thyroid papillary carcinomas cells. However, these effects were reversed by upregulation of miR-24-3p. Further exploration showed that the promoted effects of miR-24-3p mimics on thyroid papillary carcinomas cells were suppressed by enhancing p27kip1 expression. Meanwhile, MIR22HG induced p27kip1 expression by binding miR-24-3p in thyroid papillary carcinomas. CONCLUSIONS: MIR22HG inhibited cell growth through modulating p27kip1 by decreasing miR-24-3p expression in thyroid papillary carcinomas, providing a new modulate mechanism and therapeutic targets in thyroid papillary carcinomas.
机译:目的:探讨ncRNA(MIR22HG)在甲状腺乳头状癌中的潜在机制。病人与方法:从广西医科大学附属第一医院接受口腔外科手术的患者中收集40对甲状腺乳头状癌组织和相邻的正常组织。应用qRT-PCR检测MIR22HG,miR-24-3p和p27kip1在组织和细胞中的表达。 Western印迹用于测量组织和细胞中p27kip1的蛋白质水平。 Kaplan-Meier图用于分析甲状腺乳头状癌的总生存率。皮尔逊相关性分析用于分析MIR22HG,miR-24-3p和p27kip1表达之间的相关性。流式细胞仪检测细胞凋亡。 Transwell测定法用于评估细胞迁移和侵袭能力。应用荧光素酶报告基因检测法验证了甲状腺乳头状癌中MIR22HG,miR-24-3p和p27kip1之间的分子关系。结果:在甲状腺乳头状癌和细胞中,LncRNA MIR22HG和p27kip表达较低,而miR-24-3p表达较高。 MIR22HG的过表达抑制甲状腺乳头状癌细胞的细胞增殖,迁移和侵袭,而促进细胞凋亡。但是,这些作用被miR-24-3p的上调所逆转。进一步的研究表明,miR-24-3p模拟物对甲状腺乳头状癌细胞的促进作用可通过增强p27kip1表达来抑制。同时,MIR22HG通过结合miR-24-3p在甲状腺乳头状癌中诱导p27kip1表达。结论:MIR22HG通过降低甲状腺乳头状癌中miR-24-3p的表达来调节p27kip1,从而抑制细胞生长,为甲状腺乳头状癌提供了新的调控机制和治疗靶点。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号