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首页> 外文期刊>Kaohsiung Journal of Medical Sciences >Long noncoding RNAs SET-binding factor 2-antisense RNA1 promotes cell growth through targeting miR-431-5p/CDK14 axis in human papillary thyroid cancer
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Long noncoding RNAs SET-binding factor 2-antisense RNA1 promotes cell growth through targeting miR-431-5p/CDK14 axis in human papillary thyroid cancer

机译:长度非致rnas设定结合因子2-反义RNA1通过靶向miR-431-5p / cdk14轴在人乳头状甲状腺癌中促进细胞生长

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摘要

Papillary thyroid cancer (PTC) is a frequent thyroid malignancy. With the significant regulatory role in tumor progression, more attention has been employed to investigate mechanism of long noncoding RNAs (lncRNAs) in progression of PTC. We prospectively explored the mechanism whereby lncRNA SET-binding factor 2-antisense RNA1 (SBF2-AS1) is implicated in pathogenesis of PTC. First, differentially expressed SBF2-AS1 between PTC and normal adjacent thyroid tissues was determined, and result indicated a higher SBF2-AS1 expression in PTC tissues than adjacent normal tissues. Moreover, highly SBF2-AS1 expression predicted a poor prognosis in PTC patients. Second, SBF2-AS1 overexpression promoted cell viability and cycle of PTC, while inhibited cell apoptosis. However, SBF2-AS1 downregulation reduced viability and cycle, while promoted cell apoptosis. Moreover, SBF2-AS1 could bind with miR-431-5p and showed negative correlation with miR-431-5p in PTC patients. Furthermore, miR-431-5p bind with cyclin-dependent kinase (CDK) 14 and showed negative correlation with CDK14 in PTC patients. Finally, overexpression of CDK14 counteracted with the inhibitory role of SBF2-AS1 downregulation on cell viability, cycle, and apoptosis of PTC. In conclusion, SBF2-AS1 exhibited oncogenic property in PTC, and knockdown of SBF2-AS1 could be a therapeutic strategy for PTC.
机译:乳头状甲状腺癌(PTC)是常心甲状腺恶性肿瘤。在肿瘤进展中具有显着的监管作用,已经采用了更多关注来研究PTC进展中长的非分量RNA(LNCRNA)的机制。我们预期探索了LNCRNA设定结合因子2-反义RNA1(SBF2-AS1)的机制涉及PTC的发病机制。首先,确定PTC和正常相邻的甲状腺组织之间的差异表达的SBF2-AS1,结果表明了PTC组织中的较高SBF2-AS1表达,而不是相邻的正常组织。此外,高度SBF2-AS1表达预测PTC患者的预后差。其次,SBF2-AS1过表达促进了PTC的细胞活力和循环,同时抑制细胞凋亡。然而,SBF2-AS1下调降低活力和循环,同时促进细胞凋亡。此外,SBF2-AS1可以与miR-431-5P结合,并与PTC患者中的miR-431-5p与miR-431-5p结合。此外,miR-431-5p与细胞周期蛋白依赖性激酶(CDK)14结合,并与PTC患者的CDK14显示出负相关性。最后,CDK14的过度表达抵消了SBF2-AS1下调对PTC细胞活力,循环和凋亡的抑制作用。总之,SBF2-AS1在PTC中表现出致癌性质,SBF2-AS1的敲低可以是PTC治疗策略。

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