MicroRNA-133a acts as a tumour suppressor in breast cancer through targeting LASP1 Retraction in /10.3892/or.2022.8330

Sui,Yanmin; Zhang,Xiaolei; Yang,Honglan; Wei,Wei; Wang,Minglin

doi:10.3892/or.2017.6114

MicroRNA-133a acts as a tumour suppressor in breast cancer through targeting LASP1

Retraction in: /10.3892/or.2022.8330

Authors:
- Yanmin Sui
- Xiaolei Zhang
- Honglan Yang
- Wei Wei
- Minglin Wang
View Affiliations

Affiliations: Department of Oncology, Dongying People's Hospital, Dongying, Shandong 257091, P.R. China
Published online on: November 27, 2017 https://doi.org/10.3892/or.2017.6114
Pages: 473-482
Copyright: © Sui et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Many microRNAs (miRs) have been demonstrated to play promoting or tumor suppressive roles in human cancers including breast cancer. However, the molecular mechanism of miR-133a underlying the malignant progression of breast cancer still remains obscure. In the present study we observed that the expression of miR-133a was significantly downregulated in breast cancer tissues and cell lines, when compared with adjacent non-tumor tissues and normal breast cell line, respectively. Reduced miR-133a levels were significantly associated with advanced clinical stage, lymph node metastasis, as well as shorter survival time of patients with breast cancer. Restoration of miR-133a expression led to significant decrease in the proliferation, migration, and invasion of SK-BR-3 and MDA-MB-231 cells in vitro, as well as in tumor xenograft growth in nude mice. Luciferase reporter gene assay data identified LASP1 as a target gene of miR-133a, and the expression of LASP1 was negatively regulated by miR-133a in breast cancer cells. LASP1 was significantly upregulated in breast cancer tissues and cell lines, and its upregulation was significantly associated with disease progression. siRNA-induced LASP1 downregulation caused a significant reduction in breast cancer cell proliferation, migration and invasion. Furthermore, overexpression of LASP1 impaired the suppressive effects of miR-133a upregulation on the proliferation, migration and invasion of SK-BR-3 and MDA-MB-231 cells. In summary, the present study demonstrates that miR-133a acts as a tumor suppressor in breast cancer partly at least via targeting LASP1, and thus suggests that the miR-133a/LASP1 axis may become a potential therapeutic target for breast cancer.

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