P2Y2 receptor as a favorable predictor of gastric cancer.
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TL;DR
P2Y2R activation promotes GC progression may be related to PKC/Src and ERK signaling, indicating that P2Y2R may serve as a new molecular target for GC prevention and treatment.
OpenAlex 토픽 ·
Adenosine and Purinergic Signaling
Cancer, Stress, Anesthesia, and Immune Response
Inflammatory mediators and NSAID effects
P2Y2R activation promotes GC progression may be related to PKC/Src and ERK signaling, indicating that P2Y2R may serve as a new molecular target for GC prevention and treatment.
APA
Yu-qing Wu, Wen-long Wang (2026). P2Y2 receptor as a favorable predictor of gastric cancer.. Tissue & cell, 99, 103278. https://doi.org/10.1016/j.tice.2025.103278
MLA
Yu-qing Wu, et al.. "P2Y2 receptor as a favorable predictor of gastric cancer.." Tissue & cell, vol. 99, 2026, pp. 103278.
PMID
41418432 ↗
Abstract 한글 요약
[BACKGROUND] Gastric cancer (GC) prevention and treatment have always been a difficult problem to solve. Therefore, mining the molecular genes related to the progression of GC and predicting the progression of GC has important clinical significance. Therefore, this study investigated whether the P2Y2 receptor (P2Y2R) has a certain effect on GC.
[METHODS] The correlation data of P2Y2R and GC tissues from public databases was collected, and the relationship between P2Y2R and the survival and prognosis of GC patients was analyzed. Moreover, the expression of P2Y2R in GC cells AGS, MGC803, HGC27 and normal GES-1 was detected by Western-blotting. Cell scratch, Transwell invasion and YF phalloidin assays were used to investigate the effects of P2Y2R on migration and invasion of GC cells.
[RESULTS] P2Y2R was highly expressed in GC tissues and was negatively correlated with poor survival and prognosis of patients with GC. Activation of the P2Y2R by UTP promoted the migration and invasion of GC cells. However, the P2Y2R-specific antagonist AR-C118925XX inhibited the migration and invasion of GC cells. In addition, P2Y2R activation enhanced cytoskeletal stress changes in GC cells and promoted GC motility, while inhibition of its activity yielded the opposite effect. In addition, activation of P2Y2R increased the expression levels of p-PKC, p-Src, and p-ERK1/2, while AR-C118925XX treatment significantly decreased the expression levels of p-PKC, p-Src, and p-ERK1/2.
[CONCLUSION] High expression of P2Y2R is negatively correlated with survival and prognosis of GC patients. P2Y2R activation promotes GC progression may be related to PKC/Src and ERK signaling, indicating that P2Y2R may serve as a new molecular target for GC prevention and treatment.
[METHODS] The correlation data of P2Y2R and GC tissues from public databases was collected, and the relationship between P2Y2R and the survival and prognosis of GC patients was analyzed. Moreover, the expression of P2Y2R in GC cells AGS, MGC803, HGC27 and normal GES-1 was detected by Western-blotting. Cell scratch, Transwell invasion and YF phalloidin assays were used to investigate the effects of P2Y2R on migration and invasion of GC cells.
[RESULTS] P2Y2R was highly expressed in GC tissues and was negatively correlated with poor survival and prognosis of patients with GC. Activation of the P2Y2R by UTP promoted the migration and invasion of GC cells. However, the P2Y2R-specific antagonist AR-C118925XX inhibited the migration and invasion of GC cells. In addition, P2Y2R activation enhanced cytoskeletal stress changes in GC cells and promoted GC motility, while inhibition of its activity yielded the opposite effect. In addition, activation of P2Y2R increased the expression levels of p-PKC, p-Src, and p-ERK1/2, while AR-C118925XX treatment significantly decreased the expression levels of p-PKC, p-Src, and p-ERK1/2.
[CONCLUSION] High expression of P2Y2R is negatively correlated with survival and prognosis of GC patients. P2Y2R activation promotes GC progression may be related to PKC/Src and ERK signaling, indicating that P2Y2R may serve as a new molecular target for GC prevention and treatment.
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