Abstract
We read with great interest the article by Ma et al . (1), which investigated the role of N 6 -methyladenosine (m 6 A) modification in hepatocellular carcinoma (HCC) and the mechanism of methyltransferase-like 14 (METTL14) involved in the progression of liver cancer. The authors found a decreased m 6 A level in HCC compared with peritumor and normal specimens. They discovered that depleted METTL14 regulated the recognition and binding of DGCR8 and pri-miR-126 via m 6 A modification, suppressing the miR-126 expression and causing HCC metastasis. In contrast, Chen et al . (2) reported a significant increase of m 6 A level in HCC (data not shown). It was confirmed that METTL14 was not significantly decreased in HCC. They also demonstrated the promoting effect of METTL14 in liver cancer cell proliferation and migration.
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