Abstract
Background/aimEvidence is increasing that microRNAs (miRNAs) are essential for breast homeostasis and normal development. Dysregulation of these small molecules is involved with different diseases especially cancers. In this study, the miR-86-5p was induced in breast cancer cells (MDA-MB-231) and the effect of miR-86-5p replacement on the expression level of VEGF, FOX, MMP3, SIRT1, and OLFM4 genes was investigated. Material and methodsThe miR-86-5p mature sequence was designed, synthesized and transfected into the MDA-MB-231 cells via jetPRIME® transfection reagent. The optimal concentration of miRNA was determined using qRT-PCR post-transfection. MTT assay was performed to evaluate the cell toxicity of miR-86-5p replacement. For finding the role of miR-86-5p in apoptosis, the annexin V/Propidium iodid (PI) assay was performed by flow cytometry analysis. A wound-healing assay (scratch assay) was performed to assess the effect of miR-86-5p on cell migration. The qRT-PCR method was used for measuring the expression level of miR-86-5p, VEGF, FOX, SIRT1, MMP3, and OLFM4. ResultsThe results showed that the optimal concentration of miRNA was 7.5 nM. The result of MTT and apoptosis assays revealed that miR-86-5p decreased cell viability and induced apoptosis. The wound healing assays showed that the miR-86-5p inhibited cell migration. Our results also showed that the miR-86-5p reduced VEGF, MMP3, OLFM4, and SIRT1 expression compared to the negative control cells. Thus, the miR-486 may act as a tumor suppressor and plays a vital role in cell apoptosis, cell growth and migration during breast cancer development. Our results showed that miR-86-5p could be a promising candidate to be used as a therapeutic molecule in target therapy based on microRNA replacement in breast cancer.
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.
