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miR-124 通过靶向宫颈癌细胞中的amotL1 抑制血管生成拟态和细胞迁移。

MiR-124 represses vasculogenic mimicry and cell motility by targeting amotL1 in cervical cancer cells.

机构信息

Tianjin Life Science Research Center and School of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, China.

The Department of Laboratory Animal Science and Technology, Tianjin Medical University, Tianjin 300070, China.

出版信息

Cancer Lett. 2014 Dec 1;355(1):148-58. doi: 10.1016/j.canlet.2014.09.005. Epub 2014 Sep 11.

DOI:10.1016/j.canlet.2014.09.005
PMID:25218344
Abstract

miRNAs have extensive functions in differentiation, metabolism, programmed cell death, and tumor metastasis by post-transcriptional regulation. Vasculogenic mimicry is an important pathway in tumor metastasis. Many factors can regulate vasculogenic mimicry, including miRNAs. In previous studies, miR-124 was found to repress proliferation and metastasis in different types of cancers, but whether it functions in cervical cancer remained unknown. Here, we demonstrate that miR-124 can repress vasculogenic mimicry, migration and invasion in HeLa and C33A cells in vitro. Furthermore, we reveal that the effect of miR-124 on vasculogenic mimicry, migration and invasion results from its interaction with AmotL1. MiR-124 regulates AmotL1 negatively by targeting its 3'untranslated region (3'UTR). We found that miR-124 can repress the EMT process. Together, these results improve our understanding of the function of miR-124 in tumor metastasis and will help to provide new potential target sites for cervical cancer treatment.

摘要

miRNAs 通过转录后调控在分化、代谢、细胞程序性死亡和肿瘤转移中发挥广泛作用。血管生成拟态是肿瘤转移的重要途径。许多因素可以调节血管生成拟态,包括 miRNAs。在以前的研究中,miR-124 被发现可以抑制不同类型癌症的增殖和转移,但它在宫颈癌中的作用尚不清楚。在这里,我们证明 miR-124 可以抑制体外 HeLa 和 C33A 细胞中的血管生成拟态、迁移和侵袭。此外,我们揭示了 miR-124 对血管生成拟态、迁移和侵袭的影响是由于其与 AmotL1 的相互作用。miR-124 通过靶向 AmotL1 的 3'UTR 负调控 AmotL1。我们发现 miR-124 可以抑制 EMT 过程。总之,这些结果提高了我们对 miR-124 在肿瘤转移中的功能的理解,并将有助于为宫颈癌治疗提供新的潜在靶点。

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