1. Adenosine interaction with adenosine receptor A2a promotes gastric cancer metastasis by enhancing PI3K–AKT–mTOR signaling
- Author
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Zhaoying Wu, Jun Song, En Xu, Wenxian Guan, Min Feng, Linsen Shi, Shangce Du, Shichao Ai, and Ji Miao
- Subjects
Adult ,Male ,Adenosine ,Epithelial-Mesenchymal Transition ,Receptor, Adenosine A2A ,Biology ,Phosphatidylinositol 3-Kinases ,03 medical and health sciences ,0302 clinical medicine ,Cell Movement ,Stomach Neoplasms ,Cell Line, Tumor ,Tumor Microenvironment ,medicine ,Humans ,Neoplasm Metastasis ,Molecular Biology ,Protein kinase B ,PI3K/AKT/mTOR pathway ,Aged ,Cell Proliferation ,030304 developmental biology ,Aged, 80 and over ,0303 health sciences ,Tumor microenvironment ,TOR Serine-Threonine Kinases ,Receptors, Purinergic P1 ,Cell migration ,Articles ,Cell Biology ,Middle Aged ,Signaling ,Gene Expression Regulation, Neoplastic ,Adenosine Receptor A2a ,Tumor progression ,030220 oncology & carcinogenesis ,Cancer research ,Female ,Signal transduction ,Proto-Oncogene Proteins c-akt ,Signal Transduction ,medicine.drug - Abstract
The accumulation of adenosine in the tumor microenvironment is associated with tumor progression in many cancers. However, whether adenosine is involved in gastric cancer (GC) metastasis and progression, and the underlying molecular mechanism, is largely unclear. In this study, we find that GC tissues and cell lines had higher A2aR levels than nontumor gastric tissues and cell lines. A2aR expression correlated positively with TNMstage, and associated with poor outcomes. Adenosine enhanced the expression of the stemness and epithelial–mesenchymal transition-associated genes by binding to A2aR. A2aR expression on GC cells promoted metastasis in vivo. The PI3K-AKT-mTOR signaling pathway was involved in adenosine-stimulated GC cell migration and invasion. Our results indicate that adenosine promotes GC cell invasion and metastasis by interacting with A2aR to enhance PI3K–AKT–mTOR pathway signaling.
- Published
- 2019
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