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GENE:

P2RY2 (Purinergic Receptor P2Y2)

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Other names: P2RY2, Purinergic Receptor P2Y2, P2U, Purinergic Receptor P2Y, G-Protein Coupled, 2, P2Y Purinoceptor 2, P2U Purinoceptor 1, P2U Receptor 1, ATP Receptor, P2RU1, P2U1, P2Y2, P2U Nucleotide Receptor, Purinergic Receptor, Purinoceptor P2Y2, P2Y2R, HP2U, P2UR
Associations
Trials
3years
AKT/GSK-3beta/VEGF signaling is involved in P2RY2 activation-induced the proliferation and metastasis of gastric cancer. (PubMed, Carcinogenesis)
Activation of P2RY2 activated AKT/GSK-3beta/VEGF signal to promote the proliferation of GC cells, and the P13/AKT signaling pathway LY294002 reversed the corresponding phenomenon, but no synergistic pharmacological properties of AR-C118925XX and LY294002 have been found. In vivo experiments showed that ATP induced tumor growth, while AR-C118925XX inhibited ATP-induced tumor growth. Our conclusion is that P2RY2 activated the AKT/GSK-3beta/VEGF signal to promote the proliferation and migration of GC, suggesting that P2RY2 may be a new potential target for the treatment of GC.
Journal
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CDH1 (Cadherin 1) • VIM (Vimentin) • GSK3B (Glycogen Synthase Kinase 3 Beta) • SNAI1 (Snail Family Transcriptional Repressor 1) • P2RY2 (Purinergic Receptor P2Y2)
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CDH1 expression • VIM expression
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LY294002
over3years
ATP Promotes Oral Squamous Cell Carcinoma Cell Invasion and Migration by Activating the PI3K/AKT Pathway via the P2Y2-Src-EGFR Axis. (PubMed, ACS Omega)
The PI3K/AKT signaling pathway was blocked by Src or EGFR inhibitor. Extracellular ATP activates the PI3K/AKT pathway through the P2Y2-Src-EGFR axis to promote OSCC invasion and migration, and thus, P2Y2 may be a potential novel target for antimetastasis therapy.
Journal
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P2RY2 (Purinergic Receptor P2Y2)