Abstract

Breast cancer is the most frequently diagnosed malignancy among women worldwide. The occurrence rate of metastasis is also increased. It’s reported that 20–30% of breast cancer patients may develop metastases after diagnosis and primary tumor treatment, and approximately 90% of cancer-related deaths are attributed to metastasis. Recently, a growing number of studies have highlighted the significant role of miR-574-5p, a member of the miRNA family, in multiple human diseases that induce apoptosis in cancer cell lines completely understood yet. the majority of studies indicated that miR-574-5p was a promoter of NSCLC development. indicated that miR-574-5p was involved in the progression and metastasis of NSCLC. The purpose of this study is to investigate the effect of miR-574-5p migration in breast cancer. Seventy tumor and adjacent non-tumor tissues were examined in the study. The effects on cell proliferation and migration were investigated with MTT assay and scratch test, respectively. The effects on cell proliferation and migration were investigated with MTT assay and scratch test, respectively. Bioinformatics analysis was performed through enrichment and hub gene finding for miRNA targets. Metastatic breast cancer, proliferation, and migration-related to overexpression of miR-574-5p. In conclusion; miR-574-5p increased in breast cancer cell lines with a role in the growth, metastasis, and migration of breast cancer.

Full Text
Paper version not known

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 call

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.