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微小RNA-10a通过靶向磷酸酶和张力蛋白同源物增强宫颈癌细胞的转移潜能。

MicroRNA‑10a enhances the metastatic potential of cervical cancer cells by targeting phosphatase and tensin homologue.

作者信息

Zeng Tianhe, Li Guiling

机构信息

Cancer Center, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430023, P.R. China.

出版信息

Mol Med Rep. 2014 Sep;10(3):1377-82. doi: 10.3892/mmr.2014.2370. Epub 2014 Jul 9.

Abstract

Cervical cancer is one of the leading causes of cancer‑related mortality worldwide. Previously, the upregulation of microRNA (miR)‑10a has been identified in human cervical cancer. The present study firstly demonstrated that miR‑10a was markedly upregulated in primary tumor tissues in patients with positive lymph node metastasis (LN+) compared with negative (LN‑) by quantitative polymerase chain reaction. miR‑10a mimics markedly enhanced cervical cancer cell migration and invasion abilities, and accordingly the miR‑10a inhibitor suppressed those functions. Furthermore, these data suggested that the phosphatase and tensin homologue (PTEN) was inhibited by miR‑10a through an miR‑10a binding site within the 3'‑untranslated region of PTEN at the posttranscriptional level, and that miR‑10a mimics promoted nuclear translocation of β‑catenin. Therefore, it was concluded that the overexpression of miR‑10a contributes to metastasis in cervical cancer by targeting PTEN. miR‑10a may therefore be used clinically as a molecular marker for patients with cervical cancer lymph node metastasis.

摘要

宫颈癌是全球癌症相关死亡的主要原因之一。此前,已在人类宫颈癌中发现微小RNA(miR)-10a上调。本研究首先通过定量聚合酶链反应证明,与淋巴结转移阴性(LN-)患者相比,淋巴结转移阳性(LN+)患者的原发性肿瘤组织中miR-10a明显上调。miR-10a模拟物显著增强了宫颈癌细胞的迁移和侵袭能力,相应地,miR-10a抑制剂抑制了这些功能。此外,这些数据表明,磷酸酶和张力蛋白同源物(PTEN)在转录后水平通过PTEN 3'-非翻译区内的miR-10a结合位点被miR-10a抑制,并且miR-10a模拟物促进了β-连环蛋白的核转位。因此,得出结论,miR-10a的过表达通过靶向PTEN促进宫颈癌转移。因此,miR-10a在临床上可作为宫颈癌淋巴结转移患者的分子标志物。

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