The hepatic microenvironment promotes lung adenocarcinoma cell proliferation, metastasis, and epithelial-mesenchymal transition via METTL3-mediated N6-methyladenosine modification of
| Autor: | Xue-Feng, Ni, Quan-Qin, Xie, Jie-Min, Zhao, Yan-Jie, Xu, Mei, Ji, Wen-Wei, Hu, Jun, Wu, Chang-Ping, Wu |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
Adenosine
Epithelial-Mesenchymal Transition Lung Neoplasms Mice Nude Adenocarcinoma of Lung YAP1 Mice Cell Line Tumor Tumor Microenvironment Animals Humans Neoplasm Invasiveness Adaptor Proteins Signal Transducing Cell Proliferation Inflammation adenocarcinoma Liver Neoplasms YAP-Signaling Proteins Methyltransferases m6A A549 Cells METTL3 liver inflammatory microenvironment Neoplasm Transplantation Transcription Factors Research Paper |
| Zdroj: | Aging (Albany NY) |
| ISSN: | 1945-4589 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|