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. 2021 Nov 11;9:781867. doi: 10.3389/fcell.2021.781867

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Copyright © 2021 Liang, Wang, Zhang, Gao, Zhou and Wang.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Mettl3-induced m⁶A modification is involved in the upregulation of LINC00106. (A), RIP-qPCR showing the stronger enrichment of m⁶A in SNU-449 and MHCC-97H cells than that in THLE-2 cell. (B), Mettl3 expression was assessed in the HCC tissues and adjacent normal liver tissues. (C), LINC00106 expression was positively correlated with Mettl3 expression in an analysis of HCC tissues. (D), qRT-PCR of LINC00106 after Mettl3 inhibition in SNU-449 cells. (E), RIP-qPCR showing the enrichment of m⁶A in SNU-449 after Mettl3 depletion. (F), The expression of LINC00106 after treatment with 2.5 μM actinomycin D for indicated times, with depletion or overexpression of Mettl3 in SNU-449 cells. (G), RIP-qPCR showing the stronger enrichment of IGF2BP1 in SNU-449 and MHCC-97H cells than that in THLE-2 cell. (H), RIP-qPCR showing the enrichment of IGF2BP1 in SNU-449 with Mettl3 knockdown. (I), The expression of LINC00106 after treatment with 2.5 μM actinomycin D for indicated times, with IGF2BP1 knockdown in SNU-449 cells (*p < 0.05, **p < 0.01).