MicroRNA-548m suppresses cell migration and invasion by targeting aryl hydrocarbon receptor in breast cancer cells

Nor, W.F.S.B.W.M. and Chung, Ivy and Mohd Said, Nur Akmarina (2021) MicroRNA-548m suppresses cell migration and invasion by targeting aryl hydrocarbon receptor in breast cancer cells. Oncology Research, 28 (6). pp. 615-629. ISSN 09650407, DOI https://doi.org/10.3727/096504020X16037933185170.

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Breast cancer is the most commonly diagnosed cancer among women and one of the leading causes of cancer mortality worldwide, in which the most severe form happens when it metastasizes to other regions of the body. Metastasis is responsible for most treatment failures in advanced breast cancer. Epithelial-mesenchymal transition (EMT) plays a significant role in promoting metastatic processes in breast cancer. MicroRNAs (miRNAs) are highly conserved endogenous short noncoding RNAs that play a role in regulating a broad range of biological processes, including cancer initiation and development, by functioning as tumor promoters or tumor suppressors. Expression of miR-548m has been found in various types of cancers, but the biological function and molecular mechanisms of miR-548m in cancers have not been fully studied. Here we demonstrated the role of miR-548m in modulating EMT in the breast cancer cell lines MDA-MB-231 and MCF-7. Expression data for primary breast cancer obtained from NCBI GEO data sets showed that miR-548m expression was downregulated in breast cancer patients compared with healthy group. We hypothesize that miR-548m acts as a tumor suppressor in breast cancer. Overexpression of miR-548m in both cell lines increased E-cadherin expression and decreased the EMT-associated transcription factors SNAI1, SNAI2, ZEB1, and ZEB2, as well as MMP9 expression. Consequently, migration and invasion capabilities of both MDA-MB-231 and MCF-7 cells were significantly inhibited in miR-548m-overexpressing cells. Analysis of 1,059 putative target genes of miR-548m revealed common pathways involving both tight junction and the mTOR signaling pathway, which has potential impacts on cell migration and invasion. Furthermore, this study identified aryl hydrocarbon receptor (AHR) as a direct target of miR-548m in breast cancer cells. Taken together, our findings suggest a novel function of miR-548m in reversing the EMT of breast cancer by reducing their migratory and invasive potentials, at least in part via targeting AHR expression. Copyright © 2021 Cognizant, LLC.

Item Type: Article
Uncontrolled Keywords: Aryl hydrocarbon receptor; Breast cancer; Epithelial-mesenchymal transition (EMT); Invasion; MicroRNA-548m; Migration
Subjects: R Medicine > R Medicine (General)
R Medicine > R Medicine (General) > Medical technology
R Medicine > RA Public aspects of medicine > RA0421 Public health. Hygiene. Preventive Medicine
Divisions: Faculty of Medicine
Faculty of Pharmacy
Faculty of Pharmacy > Department of Pharmaceutical Life Sciences
Depositing User: Ms Zaharah Ramly
Date Deposited: 27 Nov 2023 06:13
Last Modified: 29 Nov 2023 03:50
URI: http://eprints.um.edu.my/id/eprint/35808

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