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长链非编码 RNA MALAT1 通过作为 miR-508-5p 的 ceRNA 来调节 RAB14 表达促进结直肠癌进展。

Long Noncoding RNA MALAT1 Promotes Colorectal Cancer Progression by Acting as a ceRNA of miR-508-5p to Regulate RAB14 Expression.

机构信息

First Department of Oncology, Xinxiang Central Hospital, Xinxiang, 453000 Henan, China.

Department of General Surgery, Huaihe Hospital of Henan University, Kaifeng, 475000 Henan, China.

出版信息

Biomed Res Int. 2020 Dec 4;2020:4157606. doi: 10.1155/2020/4157606. eCollection 2020.

Abstract

Accumulating evidence suggested that lncRNA MALAT1 plays critical roles in the commencement and progression of malignant cancers. Nevertheless, the function of MALAT1 in colorectal cancer (CRC) remains largely unknown. In the present study, we reported that MALAT1 expression is significantly upregulated in CRC and correlated with advanced TNM stage, lymph node metastasis, and worse prognosis in patients. Functional assays revealed that MALAT1 knockdown reduced CRC cell growth and invasion abilities . Mechanistically, we discovered that MALAT1 may serve as a competing endogenous RNA (ceRNA) to miR-508-5p in CRC progression. Bioinformatics analysis and luciferase assays confirmed that RAB14 acts as a target of miR-508-5p. In addition, downregulation of RAB14 reduced the progression of CRC. Collectively, our findings indicated that MALAT1 could promote CRC progress by sponging miR-508-5p and enhancing RAB14 expression, which provides a therapeutic target in CRC treatment.

摘要

越来越多的证据表明,长链非编码 RNA MALAT1 在恶性肿瘤的发生和发展中起着关键作用。然而,MALAT1 在结直肠癌(CRC)中的功能仍知之甚少。在本研究中,我们报道 MALAT1 表达在 CRC 中显著上调,并与患者的晚期 TNM 分期、淋巴结转移和预后不良相关。功能分析表明,MALAT1 敲低可降低 CRC 细胞的生长和侵袭能力。机制上,我们发现 MALAT1 可能在 CRC 进展中作为 miR-508-5p 的竞争性内源性 RNA(ceRNA)发挥作用。生物信息学分析和荧光素酶报告基因实验证实 RAB14 是 miR-508-5p 的靶基因。此外,下调 RAB14 可降低 CRC 的进展。综上所述,我们的研究结果表明,MALAT1 可通过海绵吸附 miR-508-5p 和增强 RAB14 的表达促进 CRC 的进展,为 CRC 的治疗提供了一个潜在的治疗靶点。

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