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首页> 外文期刊>Journal of cellular physiology. >MALAT1 rs619586 polymorphism functions as a prognostic biomarker in the management of differentiated thyroid carcinoma
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MALAT1 rs619586 polymorphism functions as a prognostic biomarker in the management of differentiated thyroid carcinoma

机译：作为一个MALAT1 rs619586多态性功能预后标志物的管理分化型甲状腺癌

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This study aimed to explore the roles of miR-214 and MALAT1 rs619586 polymorphism in the control and survival of differentiated thyroid carcinoma (DTC) via Cox regression analyses. The levels of MALAT1, miR-214, and CTNNB1 in different experimental groups were compared to study the interaction among MALAT1, miR-214, and CTNNB1. MTT and colony assays were used to investigate the role of rs619586 polymorphism in cell growth. The G allele of rs619586 polymorphism obviously decreased the 5-year survival of patients with DTC. Additionally, compared with AA-genotyped patients, patients carrying the AG/GG genotypes of MALAT1 rs619586 polymorphism showed much higher levels of DTC grade and CTNNB1 expression, along with lower levels of MALAT1 and miR-214 expression. Furthermore, the transcription activity of MALAT1 was significantly lowered by the rs619586G allele or miR-214 mimic, while the miR-214 inhibitor upregulated the luciferase activity of MALAT1. Additionally, miR-214 inhibited CTNNB1 expression by targeting CTNNB1 3'-untranslated region. Finally, the G allele of MALAT1 rs619586 polymorphism apparently promoted cell proliferation. Our study indicated that miR-214 inhibited MALAT1 expression by directly binding to the G allele of MALAT1 rs619586 polymorphism, thus inhibiting CTNNB1 expression and promoting cell proliferation in the pathogenesis of DTC. Therefore, MALAT1 rs619586 polymorphism could be used to predict the prognosis of DTC.
机译：本研究旨在探讨mir - 214的角色控制和MALAT1 rs619586多态性和生存的分化型甲状腺癌通过Cox回归分析(DTC)。MALAT1, mir - 214和CTNNB1不同实验组织进行了比较研究MALAT1之间互动,mir - 214和CTNNB1。MTT和殖民地化验调查rs619586多态性在细胞生长的作用。显然rs619586 G等位基因的多态性患者的5年存活率下降DTC。病人,病人携带AG / GG基因型的MALAT1 rs619586多态性显示更高水平的DTC品位和CTNNB1表达式,低水平的MALAT1和mir - 214表达式。MALAT1活性显著降低rs619586G等位基因或mir - 214模拟,而mir - 214荧光素酶抑制剂调节MALAT1的活动。针对CTNNB1抑制CTNNB1表达式3 '非翻译区。MALAT1 rs619586多态性明显提升细胞增殖。通过直接mir - 214抑制MALAT1表达式绑定的G等位基因MALAT1 rs619586多态性,从而抑制CTNNB1表达式和促进细胞增殖DTC的发病机理。多态性可以用来预测DTC的预后。

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