Objective: Cervical cancer is one of the gynecologic tumors in the world. The main aim of this study was to elucidate the functional role of MFI2 in cervical cancer and provide novel insight into biomarkers and therapeutic strategies for cervical cancer.
Patients and methods: The relative expression level of MFI2 was examined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Cell counting kit-8 (CCK-8) assay was involved to determine the ability of cell proliferation. Flow cytometric analysis was performed to detect cell apoptosis. Transwell assay and Matrigel assay were involved to determine cell migration and invasion. Expressions of protein kinase B (AKT), phosphorylated-AKT (p-AKT), B-cell lymphoma-2 (BCL2), and BCL2-Associated X (Bax) protein levels were detected in Western blotting. Transfected cells were used to perform tumor xenograft formation assay.
Results: Our research validated that MFI2 was up-regulated in cervical cancer by qRT-PCR. Through CCK-8 assay, flow cytometric analysis, transwell assay, and Matrigel assay, we verified that MFI2 can promote cell proliferation, cell metastasis and inhibit cell apoptosis in cervical cancer. Subsequently, we used Western blotting assay to determine the alteration of protein expression of p-AKT, BCL2, and Bax. The results indicated that MFI2 may exert its function by regulating phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway. In tumor xenograft formation assay, up-regulated MFI2 accelerated tumor formation.
Conclusions: Current research elucidated that MFI2 promoted cell proliferation, cell metastasis and inhibited cell apoptosis in cervical cancer by regulating the PI3K/AKT signaling pathway. Our results may provide a novel insight into finding new therapeutic targets and biomarkers for cervical cancer.