Issue 82, 2017

MiR-138-5p targeting LIMK1 suppresses breast cancer cell proliferation and motility

Abstract

Breast cancer is the most frequently diagnosed female cancer. LIM domain kinase 1 (LIMK1) was reported to increase breast cancer progressive biological behavior and was associated with clinical breast cancer outcomes. MiRNAs are a kind of small non-coding RNA that binds the target mRNAs, leading to protein downregulation. The aim of this study was to find whether miR-138-5p could target LIMK1 in breast cancer to suppress breast cancer biological behavior. The TCGA database showed that LIMK1 was highly expressed in breast cancer. The dual-luciferase report showed that LIMK1 was a target gene of miR-138-5p. Over-expression of miR-138-5p could significantly reduce expression of LIMK1 in mRNA and the protein level. Colony formation and MTT assay showed that over-expression of miR-138-5p could suppress proliferation of breast cancer cells. Wound-healing assay and transwell assay showed that over-expression of miR-138-5p could suppress migration and invasion of breast cancer cells. In addition, over-expression of miR-138-5p could arrest breast cancer cells into the G0/G1 phase by down-regulating expression of CDK4, 6/Cyclin D1 and CDK2/Cyclin E1 compounds. In conclusion, our study showed that miR-138-5p could target LIMK1 and suppress the progressive biological behavior of breast cancer cells. Mi-138-5p targeting LIMK1 may be a new potential treatment for breast cancer.

Graphical abstract: MiR-138-5p targeting LIMK1 suppresses breast cancer cell proliferation and motility

Article information

Article type
Paper
Submitted
15 Aug 2017
Accepted
30 Oct 2017
First published
09 Nov 2017
This article is Open Access
Creative Commons BY license

RSC Adv., 2017,7, 52030-52038

MiR-138-5p targeting LIMK1 suppresses breast cancer cell proliferation and motility

D. Li, H. Song, T. Wu, D. Xie, J. Hu, J. Zhao and L. Fang, RSC Adv., 2017, 7, 52030 DOI: 10.1039/C7RA09042K

This article is licensed under a Creative Commons Attribution 3.0 Unported Licence. You can use material from this article in other publications without requesting further permissions from the RSC, provided that the correct acknowledgement is given.

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