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miR-382 通过靶向 SETD8 抑制非小细胞肺癌肿瘤进展。

miR-382 inhibits tumor progression by targeting SETD8 in non-small cell lung cancer.

机构信息

Department of Respiratory, The First Affiliated Hospital, Xi'an Jiaotong University, Xi'an, Shaanxi 710061, PR China.

出版信息

Biomed Pharmacother. 2017 Feb;86:248-253. doi: 10.1016/j.biopha.2016.12.007. Epub 2016 Dec 19.

Abstract

Previous studies showed that miR-382 plays important roles in several types of cancers. Nevertheless, its expression and function in non-small cell lung cancer (NSCLC) remains largely unknown. In this study, we found that miR-382 expression was evidently downregulated in NSCLC tissue and cell lines in comparison with the adjacent normal tissues and human bronchial epithelial cell line (16HBE). Moreover, the expression levels of miR-382 were significantly associated with last-stage and tumor metastasis in NSCLC patients. In addition, exogenous miR-382 evidently inhibited NSCLC cell proliferation, migration and invasion in vitro. We also revealed SETD8 as a direct target of miR-382 in NSCLC, and restored SETD8 partially reversed the negative effects miR-382 on NSCLC cells. In total, our study demonstrated that miR-382 dysregulated in NSCLC and involved in NSCLC tumorigenesis and metastasis by suppressing SETD8 expression, which may help to identify effective therapies for NSCLC treatment.

摘要

先前的研究表明,miR-382 在几种类型的癌症中发挥着重要作用。然而,其在非小细胞肺癌(NSCLC)中的表达和功能在很大程度上仍是未知的。在本研究中,我们发现与相邻的正常组织和人支气管上皮细胞系(16HBE)相比,miR-382 在 NSCLC 组织和细胞系中的表达明显下调。此外,miR-382 的表达水平与 NSCLC 患者的晚期和肿瘤转移显著相关。此外,外源性 miR-382 可明显抑制 NSCLC 细胞在体外的增殖、迁移和侵袭。我们还揭示了 SETD8 是 NSCLC 中 miR-382 的直接靶标,并且恢复 SETD8 部分逆转了 miR-382 对 NSCLC 细胞的负性作用。总的来说,我们的研究表明,miR-382 在 NSCLC 中失调,通过抑制 SETD8 的表达参与 NSCLC 的发生和转移,这可能有助于为 NSCLC 的治疗确定有效的治疗方法。

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