CXC趋化因子受体2在胆囊癌组织的表达及其对胆囊癌细胞侵袭迁移的影响

Expression of CXC chemokine receptor 2 in gallbladder cancer and its effect on cell invasion and migration

目的:探讨CXC趋化因子受体2(CXCR2)在胆囊癌组织中的表达及其对胆囊癌细胞侵袭迁移的影响。方法:收集2017年1月至2021年12月宁波大学附属李惠利医院手术切除的64例胆囊癌患者肿瘤组织和癌旁组织标本。采用免疫组织化学染色法检测CXCR2蛋白表达,分析其与患者临床病理特征的相关性。将胆囊癌细胞株NOZ与外源性CXC趋化因子配体5(CXCL5)共培养处理后,Transwell实验检测细胞的侵袭迁移能力。利用RNA干扰技术沉默CXCR2基因,观察其对CXCL5介导细胞侵袭迁移的影响。组间比较采用χ^(2)检验和独立样本t检验。结果:胆囊癌组织中CXCR2蛋白的阳性表达率明显高于癌旁组织[65.6%(42/64)比39.1%(25/64),χ^(2)=9.051,P<0.05]。而且,CXCR2表达与肿瘤分期(χ^(2)=9.924,P<0.05)和淋巴结转移(χ^(2)=7.182,P<0.05)显著相关。Transwell实验结果表明,CXCL5共培养组细胞的侵袭迁移能力显著高于空白对照组[(156.60±15.93)个比(68.40±7.99)个,t=11.067,P<0.05],而CXCR2敲减+CXCL5共培养组细胞的侵袭迁移能力显著低于CXCL5共培养组[(82.20±9.88)个比(156.60±15.93)个,t=8.874,P<0.05]。结论:CXCR2在胆囊癌组织中表达升高,可调控胆囊癌细胞的侵袭迁移能力。

Objective To investigate the expression of CXC chemokine receptor 2(CXCR2)in gallbladder cancer(GBC)and its effect on cell invasion and migration.Methods The surgically resected specimens of 64 GBC patients were collected in Lihuili Hospital Affiliated to Ningbo University from January 2017 to December 2021.The expression of CXCR2 protein in GBC tissues and corresponding paracancer tissues was detected by immunohistochemistry.After co-culturing of GBC cell line NOZ with exogenous CXC chemokine ligand 5(CXCL5),Transwell assay was performed to assess the cell invasion ability.Small interfering RNA was employed to silence the expression of CXCR2 gene and then the effect of CXCR2 knockdown on CXCL5-induced cell invasion was evaluated.Comparisons between groups were performed byχ^(2) test and independent sample t-test.Results The positive expression rate of CXCR2 protein in GBC tissues was significantly higher than that in paracancerous tissues[65.6%(42/64)vs.39.1%(25/64),χ^(2)=9.051,P<0.05].Furthermore,CXCR2 expression was significantly associated with tumor stage(χ^(2)=9.924,P<0.05)and lymph nodal metastasis(χ^(2)=7.182,P<0.05).Transwell assay showed that the cell invasion ability in CXCL5-treated group significantly increased than that in the blank control group[number of transmembrane cells:(156.60±15.93)cells vs.(68.40±7.99)cells,t=11.067,P<0.05],whereas the cell invasion ability in CXCR2 knockdown+CXCL5-treated group significantly decreased than that in CXCL5-treated group[number of transmembrane cells:(82.20±9.88)cells vs.(156.60±15.93)cells,t=8.874,P<0.05].Conclusion CXCR2 is overexpressed in GBC and can regulate the invasion and migration of GBC cells.