Research Paper Volume 13, Issue 3 pp 4357—4369

The hepatic microenvironment promotes lung adenocarcinoma cell proliferation, metastasis, and epithelial–mesenchymal transition via METTL3-mediated N6-methyladenosine modification of YAP1

The hepatic inflammatory microenvironment significantly increased m6A methylation and METTL3 expression in A549 and H1975 lung adenocarcinoma (LUAD) cells. (A) The hepatic inflammatory microenvironment significantly increased the level of m6A methylation in A549 and H1975 LUAD cells. (B) METTL3 mRNA expression in A549 and H1975 cells was significantly increased by the inflammatory microenvironment of the liver. (C) The Kaplan–Meir Plot database indicated that METTL3 expression in lung cancer was positively correlated with prognosis. (D) The hepatic inflammatory microenvironment significantly increased METTL3 expression in A549 and H1975 cells. (E) The hepatic inflammatory microenvironment significantly increased the activity of the METTL3 promoter in A549 and H1975 cells (*P

Figure 3. The hepatic inflammatory microenvironment significantly increased m6A methylation and METTL3 expression in A549 and H1975 lung adenocarcinoma (LUAD) cells. (A) The hepatic inflammatory microenvironment significantly increased the level of m6A methylation in A549 and H1975 LUAD cells. (B) METTL3 mRNA expression in A549 and H1975 cells was significantly increased by the inflammatory microenvironment of the liver. (C) The Kaplan–Meir Plot database indicated that METTL3 expression in lung cancer was positively correlated with prognosis. (D) The hepatic inflammatory microenvironment significantly increased METTL3 expression in A549 and H1975 cells. (E) The hepatic inflammatory microenvironment significantly increased the activity of the METTL3 promoter in A549 and H1975 cells (*P<0.05 versus the control group).