CXCR1调控STAT3信号通路对结肠癌细胞增殖凋亡的影响

Effect of CXCR1 Regulates STAT3 Signaling Pathway on Proliferation and Apoptosis of Colon Cancer Cells

目的探讨化学趋化因子受体1(CXCR1)对结肠癌细胞增殖凋亡的影响及机制。方法收集结肠癌组织和对应的癌旁组织,提取组织蛋白,Western blot法检测组织中CXCR1表达水平。以人结肠癌细胞HCT116为研究对象,细胞转染CXCR1小干扰RNA(CXCR1 siRNA组),同时转染siRNA对照组。设置对照组,对照组中只加入转染试剂。培养48h后,Western blot法检测细胞中CXCR1、Bcl-2、Bax、STAT3、p-STAT3表达水平,MTT检测细胞增殖情况,流式细胞术检测细胞凋亡情况。人结肠癌细胞与STAT3信号通路抑制剂AG490作用后,检测细胞增殖凋亡情况。结果 CXCR1在结肠癌组织中的表达水平明显高于癌旁组织(P<0.01)。CXCR1 siRNA组细胞中CXCR1、p-STAT3、Bcl-2蛋白水平和细胞存活率明显低于对照组(P<0.01)。CXCR1 si RNA组细胞中Bax水平和细胞凋亡率明显高于对照组(P<0.01)。siRNA对照组细胞中CXCR1、Bcl-2、Bax、STAT3、p-STAT3水平和细胞凋亡率、细胞存活率与对照组比较,差异均无统计学意义(P>0.05)。抑制剂作用后的细胞增殖凋亡趋势与CXCR1 siRNA组细胞相一致。结论 CXCR1在结肠癌组织中表达上调。抑制CXCR1的表达可以抑制结肠癌细胞增殖,促进结肠癌细胞凋亡,作用机制与STAT3信号通路有关。

Objective To investigate the effect and mechanism of CXCR1 on the proliferation and apoptosis of colon cancer cells. Methods The CXCR1 expression levels in the tissues of colon cancer and corresponding adjacent tissues were detected by Western blot. Human colon cancer cell HCT116 was taken as the research object. The ceils were transfected with CXCR1 small interfering RNA （ siRNA CXCR1 group）, and transfected into siRNA control （siRNA control group）. The control group was Set up, which were added into the transfection reagent. After cultured for 48h,Western blot was used to detected the expression levels of CXCR1, Bcl -2, Bax, STAT3, p - STAT3 in ceils. MTT was used to detected cell proliferation. Flow cytometry was used to detect cell apoptosis. The proliferation and apoptosis of human colon cancer cells was detected after treated with STAT3 signaling pathway inhibitor AG490. Results The expression level of CXCR1 in colon cancer tissue were significantly higher than that in adjacent tissues （P 〈 0.01 ）. The levels of CXCR1, p - STAT3, Bcl - 2 and cell survival rate in CXCR1 siRNA group were significantly lower than those in control group （P 〈 0.01 ）. Bax level and apoptosis rate in CXCR1 siRNA group were significantly higher than those in control group （ P 〈 0.01 ）. The levels of CXCR1, Bcl - 2, Bax, STAT3, p - STAT3 and cell survival rate in siRNA control group were not significantly different from the control group （ P 〉 O. 05 ）. The cell proliferation and apoptosis after the action of the inhibitor were consistent with the CXCR1 siRNA group. Conclusion CXCR1 expression was up - regulated in colon carcinoma tissues. Inhibiting the expression of CXCR1 could inhibit the proliferation of co- lon cancer cells and promote the apoptosis of colon cancer cells. The mechanism of action was related to the STAT3 signaling pathway.