Purpose: The microRNAs (miRs) control a vast number of biological and cellular processes. miR-1 has been implicated in the development and progression in different types of cancers. Nonetheless, the function and therapeutic implications of miR-1 have not been studied in breast cancer. This study was undertaken to study the role of miR-1 in human breast cancer cells.
Methods: MBA-MD-231 breast cancer line and the normal MB-157 cell line were mainly used in this research. Expression analysis was performed by qRT-PCR. Cell viability was determined by MTT assay and apoptosis was detected by acridine orange (AO)/ethidium bromide (EB) and DAPI staining. Transwell assay was used for cell migration and invasion and western blot analysis was used to determine the protein expression.
Results: miR-1 was significantly but aberrantly suppressed in breast cancer cells relative to the MB-157 normal cells. Overexpression of miR-1 in MBA-MD-231 suppressed their proliferation dose-dependently. The inhibition of MBA-MD-231 cell proliferation was found to be due to induction of apoptosis. The apoptotic cell percentage was 37.1% in miR-1 mimics transfected in comparison to 3.7% in miR-negative control (NC) transfected cells. Additionally, miR-1 also suppressed the chemosensitivity of the MBA-MD-1 breast cancer cells to cisplatin. Transwell assay showed that miR-1 overexpression suppressed the migration and invasion of the MBA-MD-231 cells. The results clearly showed that overexpression of miR-1 suppressed the phosphorylation of MEK and ERK.
Conclusion: miR-1 acts as a tumor suppressor and may exhibit therapeutic implications in the treatment of breast cancer.