目的：探究CXC类趋化因子受体2（C-X-C motif chemokine receptor, CXCR2）对胃癌细胞侵袭、迁移及凋亡等生物学特性的影响。方法：取人胃癌MGC80-3细胞和SGC-7901细胞。转染建立CXCR2过表达细胞,质粒瞬时转染和RNA干扰建立敲减细胞。蛋白质印迹实验研究蛋白质相关细胞表型变化。通过transwell侵袭及迁移实验、增殖实验（cell counting kit-8, CCK8）、流式细胞实验Annexin Ⅴ-PI双染法以及实时定量PCR等进行细胞功能、增殖、凋亡以及CXCR2 mRNA表达的检测。结果：胃癌细胞过表达CXCR2后其侵袭、迁移能力显著增强（P<0.05）,凋亡率显著降低（P<0.01）。CXCR2下调后抑制胃癌细胞的侵袭、迁移能力（P<0.05）,凋亡率显著升高（P=0.02）。CXCR2过表达的胃癌细胞中Akt的磷酸化水平显著上调。Akt磷酸化水平与凋亡抑制蛋白Bcl-2的表达水平相一致。结论：CXCR2上调后增强胃癌细胞的侵袭、迁移及抗凋亡能力。胃癌细胞中CXCR2的抗凋亡能力与CXCR2/Akt/Bcl-2通路相关。

Objective To investigate the effects of C-X-C motif chemokine receptor 2 (CXCR2) on invasion, migration and apoptosis of gastric cancer cells. Methods Gastric cancer cells MGC80-3 and SGC-7901 with upregulated CXCR2 were established by stable Lentivirus transfection. CXCR2 gene silencing cells were established by plasmid transient transfection and RNA interference. Proteins related to cell phenotype changes were detected by Western blotting. The functional changes of cells were detected by transwell invasion and migration assays. Cell proliferation was measured by CCK8 assays. Apoptosis was detected by Annexin V-PI double staining of flow cytometry. CXCR2 mRNA was detected via real-time quantitative PCR. Results Upregulation of CXCR2 in gastric cancer cells exhibited an increased ability of cells migration and invasion (P<0.05) and reduced the apoptosis rate (P<0.01). Downregulation of CXCR2 inhibited the invasion and migration ability of gastric cancer cells(P<0.05) and increased the apoptosis rate(P=0.02). Phosphorylation level of Akt in gastric cancer cells which overexpressed CXCR2 was significantly upregulated. Phosphorylation level of Akt was consistent with the expression of apoptosis inhibitor protein Bcl-2. Conclusions Upregulation of CXCR2 enhanced the ability of invasion, migration and evasion of apoptosis of gastric cancer cell. The evasion of apoptosis was associated with CXCR2/Aki/Bcl-2 pathway.