miR-328-5p inhibits MDA-MB-231 breast cancer cell proliferation by targeting RAGE

Luo,Tingting; Yan,Yueqiong; He,Qiuxia; Ma,Xiaoqian; Wang,Wei

doi:10.3892/or.2018.6353

miR-328-5p inhibits MDA-MB-231 breast cancer cell proliferation by targeting RAGE

Authors:
- Tingting Luo
- Yueqiong Yan
- Qiuxia He
- Xiaoqian Ma
- Wei Wang
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Affiliations: Department of Ultrasonography, The Third Xiangya Hospital, Central South University, Changsha, Hunan 410011, P.R. China, Department of Radiology, The Third Xiangya Hospital, Central South University, Changsha, Hunan 410011, P.R. China
Published online on: April 4, 2018 https://doi.org/10.3892/or.2018.6353
Pages: 2906-2914

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Abstract

MicroRNAs (miRNAs) are a class of short non-coding RNAs that play an important role in gene regulation and are critically involved in the pathogenesis and progression of human cancer. miR-328-5p has been reported to potentially act as a sensitising agent in breast cancer, but its other cellular functions and mechanisms remain unknown. The primary aim of the present study was to discover additional cellular functions and mechanisms of miR-328-5p in the breast cancer cell line MDA-MB-231. In the present study, miRNA microarray was used to find altered miRNAs. MTT and colony formation were used to test cell proliferation. Flow cytometry and western blotting were used to explore potential mechanisms of miR-328-5p regulating cell proliferation. A luciferase reporter assay was used to confirm target binding. miR-328-5p was revealed to be significantly upregulated after knockdown of the receptor for advanced glycosylation end products (RAGE). We also confirmed that miR-328-5p was frequently decreased in breast cancer tissues. Moreover, miR-328-5p mimics inhibited MDA-MB-231 proliferation, drug resistance and cell cycle progression. We confirmed that RAGE was a direct target of miR-328-5p. Functions of miR-328-5p in MDA-MB‑231 cells were elucidated by targeting RAGE. In conclusion, these results revealed that miR-328-5p may be considered as a tumour-suppressor factor, and promoting miR-328-5p expression could be a novel therapeutic strategy for breast cancer.

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