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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

Xue-Feng Ni1, Quan-Qin Xie2, Jie-Min Zhao1, Yan-jie Xu1, Mei Ji1, Wen-Wei Hu1, Jun Wu1, Chang-Ping Wu1
  • 1Department of Oncology, The Third Affiliated Hospital of Soochow University, Changzhou, China
  • 2Department of Gastroenterology, The Third Affiliated Hospital of Soochow University, Changzhou, China
Received: April 16, 2020Accepted: October 27, 2020Published: January 20, 2021
https://doi.org/10.18632/aging.202397

Copyright: © 2021 Ni et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

The inflammatory microenvironment plays an important role in the onset and progression of lung adenocarcinoma (LUAD), and the liver is a suitable site of metastasis for LUAD cells. However, whether the inflammatory microenvironment of the liver is conducive to the proliferation, invasion, and metastasis of LUAD cells remains unclear. In this study, we confirmed that the hepatic inflammatory microenvironment stimulated by IL-6 promoted the proliferation, migration, invasion, and epithelial–mesenchymal transition of LUAD cells, increased the m6A methylation of total RNA, and transcriptionally activated METTL3 expression. Additionally, METTL3 activated the YAP1/TEAD signaling pathway by increasing the m6A modification and expression of YAP1 mRNA. These results indicate that the hepatic inflammatory microenvironment plays a role in regulating the biological functions of LUAD cells. Further, our study identifies a molecular mechanism that may provide a new strategy for the early diagnosis, treatment, and prognosis of liver metastasis in LUAD patients.