Objective: Breast cancer is one of the most common malignant tumors in women. Despite the advances made in treatments of breast cancer, the incidence and death rates of breast cancer are still on the rise. Therefore, it is essential for us to explore the potential mechanism accounting for the malignancy of breast cancer.
Materials and methods: A lentiviral vector over-expressing miR-99a in MDA-MB-231 breast cancer cells was constructed. Cell proliferation was detected by MTT assay. Migration and invasion were measured by Scratch-wound assay and transwell assay. Direct target of miR-99a in MDA-MB-231 breast cancer cells was examined using bioinformatics and luciferase assay. The expression of endogenous insulin-like growth factor 1 receptor was quantified by qRT-PCR and Western blotting.
Results: In our study, we found that miR-99a could suppress the proliferation, migration and invasion of MDA-MB-231 cell in vitro and inhibited the growth of xeno-transplant tumor in vivo. We also found that insulin-like growth factor 1 receptor (IGF-1R) was a direct target of miR-99a. Furthermore, knockdown of endogenous IGF-1R by siRNA could mimic the effect of miR-99a over-expression.
Conclusions: Our findings demonstrated that miR-99a could inhibit the malignancy of breast cancer cell by directly down-regulation of IGF-1R. These results indicated that miR-99a may be an important biomarker for prognosis and anticancer therapy in breast cancer in the future.