METTL14 suppresses the metastatic potential of HCC by modulating m A-dependent primary miRNA processing.

M A modification has been implicated in many biological processes. However, its role in cancer has not been well studied. Here, we demonstrate that m A modifications are decreased in HCC, especially in metastatic HCC, and that METTL14 is the main factor involved in aberrant m A modification. Moreover, METTL14 down-regulation acts as an adverse prognosis factor for recurrence-free survival (RFS) of HCC and is significantly associated with tumour metastasis in vitro and in vivo. We confirm that METTL14 interacts with the microprocessor protein DGCR8 and positively modulates the pri-miR126 process in an m A-dependent manner. Further experiments show that miR-126 inhibits the repressing effect of METTL14 in tumour metastasis.,Our studies reveal an important role of METTL14 in tumour metastasis and provide a fresh view on m A modification in tumour progression. This article is protected by copyright. All rights reserved.