Abstract
Dysregulated microRNAs (miRNAs) serve vital roles in the progression and prognosis of breast cancer. miR-623 has been reported to influence the progression of numerous other cancers, such as lung adenocarcinoma and hepatocellular carcinoma, however, its role in breast cancer remains unclear. In the present study, the mRNA expression of miR-623 was studied in 121 pairs of breast cancer and adjacent normal tissues and cultured cell lines by reverse-transcription quantitative PCR. The association between miR-623 expression and clinical characteristics or the overall survival rate of patients was investigated by the χ2 test or Cox regression analysis, respectively. The role of miR-623 in cell proliferation, migration and invasion of breast cancer cells was evaluated by cell transfection to regulate miR-623 expression and the CCK8 and Transwell assays, respectively. miR-623 was downregulated in breast cancer tissues and cell lines compared with normal tissues and breast epithelial cell lines. The χ2 test demonstrated that the downregulation of miR-623 was associated with the tumor node metastasis (TNM) stage of patients with breast cancer. miR-623 and TNM stage were considered as two independent prognostic factors for breast cancer. Additionally, cell proliferation, migration, and invasion of breast cancer cells were promoted by the downregulation of miR-623, while upregulation of miR-623 led to inhibition of the aforementioned processes. Downregulation of miR-623 in breast cancer is associated with the development of breast cancer and indicates a poor prognosis of patients. The downregulation of miR-623 promotes cell proliferation, migration and invasion of breast cancer. The findings of the present study indicate that miR-623 functions as a prognosis biomarker and a tumor suppressor in breast cancer, which provides a potential therapeutic target for patients with breast cancer.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: 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.