miR-543 inhibites cervical cancer growth and metastasis by targeting TRPM7.

Dysregulation of miR-543 has been implicated to play crucial roles in various human cancers. However, the function of miR-543 involved in cervical cancer (CC) progress remains largely unknown. Thus, this study aimed to explore the potential role of miR-543 and the underlying mechanisms in human CC. In this study, we found that miR-543 was significantly downregulated in 69 CC tissue samples and cell lines when compared to adjacent normal tissues and cell line. Decreased miR-543 was closely correlated with poor clinicopathological parameters including larger tumor size, late FIGO stage and lymph node metastasis. Overexpression of miR-543 in CC cell lines remarkably inhibited cell proliferation, invasion and migration, caused cell cycle arrest, promoted apoptosis in vitro, and suppressed tumor growth in vivo, whereas miR-543 inhibitor showed the opposite effect. Dual-luciferase assay validated that 3'-untranslated region (UTR) of transient receptor potential melastatin 7 (TRPM7) was a direct binding site of miR-543. Rescue experiments showed that restoration of TRPM7 expression partially reversed the miR-543-mediated inhibition of proliferation and invasion in CC cells. Further studies confirmed that P13K/AKT and p38/MAPK signaling was involved in miR-543/TRPM7 axis mediated CC progression. Thus, these findings demonstrated the tumor suppressor role of miR-543 on CC progression, which might serve as a potential biomarker for CC diagnosis and therapy.