Abstract
MicroRNAs (miRNAs), as key negative regulators of gene expression, are closely related to tumor occurrence and progression. miR-194-5p (miR-194-1) has been shown to play a regulatory role in various cancers however, its biological function and mechanism of action in breast cancer have not yet been well explored. In this study, we use the UALCAN and LinkedOmics databases to analyze transcription expression in The Cancer Genome Atlas Breast Invasive Carcinoma (TCGA-BRCA). The epithelial-mesenchymal transition status of breast cancer cells was evaluated by wound-healing assay, trans-well assays, and gelatin zymography, while protein expression was assessed by Western blotting. miR-194-5p expression was found to be up-regulated in breast cancer clinical specimens but down-regulated in the triple-negative breast cancer (TNBC) cell line MDA-MB-231 and breast cancer clinical specimens in The Cancer Genome Atlas (TCGA). miR-194-5p significantly inhibited the expression of the epithelial marker ZO-1 and increased the expression of mesenchymal markers, including ZEB-1 and vimentin, in MDA-MB-231 cells. miR-194-5p significantly reduced the gelatin-degrading activity of matrix metalloproteinase-2 (MMP-2) and MMP-9 in zymography assays. In MDA-MB-231 cells and TCGA patient samples, ZEB-1 expression was significantly inversely correlated with miR-194-5p expression. High levels of miR-194-5p were associated with good overall survival. miR-194-5p regulates epithelial–mesenchymal transition (EMT) in TNBC. Our findings suggest that miR-194-5p functions as a tumor biomarker in breast cancer, providing new insights for the study of breast cancer development and metastasis.
Highlights
Breast cancer is a leading cause of death and the most commonly diagnosed cancer in women worldwide
A forest plot displaying the number of tumor and normal samples, the area under the receiver operating characteristic (ROC) curve (AUC), and 95% confidence interval (CI) of the AUC for each cancer type in The Cancer Genome Atlas (TCGA) was used to visualize the results of the pan-cancer ROC analysis by CancerMIRNome bioinformatic analysis (Figure 1B) [23]
Our results suggested that miR-194-5p is down-regulated in triple-negative breast cancer (TNBC). miR-194-5p inhibited the migration ability of metastatic MDA-MB-231 cells
Summary
Breast cancer is a leading cause of death and the most commonly diagnosed cancer in women worldwide. Primary breast cancer cells expressing estrogen receptors (ER) or progesterone receptors (PR) can be treated with hormone therapy. Triple-negative breast cancer (TNBC) is characterized by an absence of the estrogen receptor (ER), the progesterone receptor (PR), and HER-2 (human epidermal growth factor receptor 2). The roles of miRNAs have been increasingly associated with breast cancer metastasis. The metastasis and spread of cancer cells are the main reasons for the recurrence and death of cancer patients, as well as increased difficulty of treatment. ZEB1 expression exhibits a repressive role and contributes to anti-cancer drug resistance [21,22]. The expression level of miR-194-5p is examined in breast cancer cell lines and clinical tissues. The potential miR-194-5p-directed target genes are identified and characterized, and the action mechanism of miR-194-5p in breast cell migration is investigated. A forest plot displaying the number of tumor and normal samples, the area under the ROC curve (AUC), and 95% confidence interval (CI) of the AUC for each cancer type in TCGA was used to visualize the results of the pan-cancer ROC analysis by CancerMIRNome bioinformatic analysis (Figure 1B) [23]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
