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微小 RNA-124 通过负向调控氯离子通道蛋白 1 抑制肝癌细胞的迁移和侵袭。

MicroRNA‑124 negatively regulates chloride intracellular channel 1 to suppress the migration and invasion of liver cancer cells.

机构信息

Department of Bioengineering, Zhuhai Campus of Zunyi Medical University, Zhuhai, Guangdong 519041, P.R. China.

The Department of Integrative Physiology and Neuroscience, Washington State University, Pullman, WA 99163, USA.

出版信息

Oncol Rep. 2019 Oct;42(4):1380-1390. doi: 10.3892/or.2019.7250. Epub 2019 Jul 25.

DOI:10.3892/or.2019.7250
PMID:31364737
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6718097/
Abstract

The dysregulation of microRNAs (miRNAs) is associated with the development and progression of a variety of cancers, including liver cancer. Aberrant expression of miRNA (miR)‑124 has been demonstrated in liver cancer, but its functional mechanism in liver cancer is still largely unknown. Metastasis of liver cancer is one of the most common causes of mortality. The present study showed that miR‑124 inhibited the proliferation, migration and invasion of liver cancer cells. Furthermore, chloride intracellular channel 1 (CLIC1) was identified as a novel target of miR‑124 in liver cancer cells. Overexpression of miR‑124 reduced CLIC1 expression at both the protein and mRNA levels in liver cancer cells. Downregulation of CLIC1 decreased the migration and invasion of liver cancer cells without affecting cell proliferation. Taken together, these results showed that CLIC1 is a critical target for miR‑124‑mediated inhibitory effects on cell migration and invasion. Thus, miR‑124 or suppression of CLIC1 may have diagnostic value and therapeutic potential for the treatment of human liver cancer.

摘要

miRNAs(miRNA)的失调与多种癌症的发展和进展有关,包括肝癌。已经证明 miRNA(miR)-124 在肝癌中表达异常,但它在肝癌中的功能机制在很大程度上仍不清楚。肝癌的转移是导致肝癌患者死亡的最常见原因之一。本研究表明,miR-124 抑制肝癌细胞的增殖、迁移和侵袭。此外,氯离子通道 1(CLIC1)被鉴定为肝癌细胞中 miR-124 的一个新靶标。在肝癌细胞中过表达 miR-124 可降低 CLIC1 的蛋白和 mRNA 水平。下调 CLIC1 可减少肝癌细胞的迁移和侵袭,而不影响细胞增殖。综上所述,这些结果表明 CLIC1 是 miR-124 抑制细胞迁移和侵袭的关键靶标。因此,miR-124 或抑制 CLIC1 可能对人类肝癌的诊断和治疗具有潜在的价值。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cb1/6718097/3cccdb404aab/or-42-04-1380-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cb1/6718097/1e7c9844a678/or-42-04-1380-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cb1/6718097/aeb7a2d9f0f4/or-42-04-1380-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cb1/6718097/174aa3e7ff80/or-42-04-1380-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cb1/6718097/3cccdb404aab/or-42-04-1380-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cb1/6718097/1e7c9844a678/or-42-04-1380-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cb1/6718097/aeb7a2d9f0f4/or-42-04-1380-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cb1/6718097/174aa3e7ff80/or-42-04-1380-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cb1/6718097/3cccdb404aab/or-42-04-1380-g05.jpg

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