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长链非编码 RNA-KAT7 通过表观遗传途径负调控 miR-10a 参与非小细胞肺癌。

LncRNA-KAT7 Negatively Regulates miR-10a Through an Epigenetic Pathway to Participate in Nonsmall Cell Lung Cancer.

机构信息

Department of Respiratory Medicine, Affiliated Heping Hospital of Changzhi Medical College, Changzhi City, P.R. China.

出版信息

Cancer Biother Radiopharm. 2021 Jun;36(5):441-445. doi: 10.1089/cbr.2019.3228. Epub 2020 May 18.

Abstract

LncRNA-KAT7 is a recently identified tumor suppressor in colorectal cancer, whereas its roles in other malignancies remain unclear. This study aimed to investigate the roles of KAT7 in nonsmall cell lung cancer (NSCLC). The results showed that KAT7 was downregulated in NSCLC and predicted poor survival. KAT7 negatively correlated with miR-10a in NSCLC. In NSCLC cells, overexpression of KAT7 led to downregulated miR-10a, whereas silencing of KAT7 led to upregulated miR-10a. Methylation-specific polymerase chain reaction revealed that KAT7 positively regulated the methylation of miR-10a. Cell proliferation assay showed that overexpression of miR-10a led to increased proliferation rate of NSCLC cells. In addition, overexpression of KAT7 played an opposite role and reduced the effects of the overexpression of miR-10a. In conclusion, KAT7 negatively regulates miR-10a through epigenetic mechanisms to participate in NSCLC cell proliferation.

摘要

长链非编码 RNA-KAT7 是结直肠癌中最近发现的一种肿瘤抑制因子,但其在其他恶性肿瘤中的作用尚不清楚。本研究旨在探讨 KAT7 在非小细胞肺癌(NSCLC)中的作用。结果表明,KAT7 在 NSCLC 中下调,并预测预后不良。KAT7 与 NSCLC 中的 miR-10a 呈负相关。在 NSCLC 细胞中,过表达 KAT7 导致 miR-10a 下调,而沉默 KAT7 导致 miR-10a 上调。甲基化特异性聚合酶链反应显示 KAT7 正向调节 miR-10a 的甲基化。细胞增殖试验表明,过表达 miR-10a 导致 NSCLC 细胞增殖率增加。此外,过表达 KAT7 发挥相反的作用,并降低了过表达 miR-10a 的作用。总之,KAT7 通过表观遗传机制负调控 miR-10a 参与 NSCLC 细胞增殖。

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