MicroRNA-671-3p inhibits the development of breast cancer: A study based on in vitro experiments, in-house quantitative polymerase chain reaction and bioinformatics analysis

MicroRNA-671-3p抑制乳腺癌的发展:一项基于体外实验、内部定量聚合酶链式反应和生物信息学分析的研究

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作者:Dan-Dan Xiong, Hao Chen, Rong-Quan He, Ai-Hua Lan, Jin-Cai Zhong, Gang Chen, Zhen-Bo Feng, Kang-Lai Wei

Abstract

MicroRNAs (miRNAs or miRs) are highly conserved small noncoding RNA molecules involved in gene regulation. An increasing number of studies have demonstrated that miRNAs act as oncogenes or antioncogenes in various types of cancer, including breast cancer (BC). However, the exact role of miR‑671‑3p in BC has not yet been reported. In the present study, in vitro experiments were implemented to explore the effects of miR‑671‑3p on the proliferation and apoptosis of BC cells, and reverse transcription‑quantitative polymerase chain reaction was conducted using in‑house clinical BC samples to address the expression level and clinical value of miR‑671‑3p in BC. Simultaneously, miR‑671‑3p target genes were collected, and subsequent bioinformatics analyses were executed to probe the potential signaling pathway through which miR‑671‑3p influenced the occurrence and progression of BC. According to the results, the expression level of miR‑671‑3p was lower in BC tissues compared with that in adjacent non‑tumorous tissues (P=0.048), and the area under the curve was 0.697 (95% confidence interval=0.538‑0.856), with a sensitivity and specificity of 0.818 and 0.579, respectively. Forced miR‑671‑3p expression in the BC cell line MDA‑MB‑231 evidently arrested cell proliferation and induced cell apoptosis. Furthermore, in silico enrichment analyses suggested that miR‑671‑3p may be involved in the initiation and progression of BC through the targeting of genes associated with the Wnt signaling pathway. In conclusion, the present study findings suggested that miR‑671‑3p may function as a tumor suppressor in BC by influencing the Wnt signaling cascade, which provides a prospective molecular target for the therapy of BC.

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