Abstract
Meningioma-associated protein 30 (MAC30) is a vital modulator of malignant transformation in numerous cancers. Yet, the involvement of MAC30 in nasopharyngeal carcinoma (NPC) is undetermined. This study was devoted to the study of the function of MAC30 in NPC, along with the molecular mechanism of its involvement in disease progression. This study showed an elevated level of MAC30 in NPC tissues and cell lines. MAC30 silencing impeded the proliferation, colony formation, and invasion of NPC cells, while MAC30 upregulation had the opposite effects. MAC30 regulated the Wnt/β-catenin pathway via affecting the protein kinase B (Akt)/glycogen synthase kinase-3β axis. Akt inhibition markedly abrogated the MAC30-mediated activation of the Wnt/β-catenin pathway. Restoration of β-catenin reversed MAC30 silencing-induced tumor-inhibiting effects. Knockdown of MAC30 weakened the tumorigenic potential of NPC cells in vivo. This study elucidates the fact that inhibition of MAC30 produces antitumor effects in NPC via affecting the Akt/Wnt/β-catenin pathway.
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