I-TAC/CXCR3生物轴对甲状腺癌病理生物学行为的影响  

Effect of I-TAC/CXCR3 biological axis on pathobiological behavior of thyroid carcinoma

作　　者：卜春艳 顾桂源 孟宇澄 曹斌 BU Chun-yan;GU Gui-yuan;MENG Yu-cheng;CAO Bin(Department of Pathology,Hai′an People′s Hospital,Hai'an 226600,China;Department of Nuclear Medicine,Hai′an People′s Hospital,Hai'an 226600,China)

机构地区：[1]海安市人民医院病理科,江苏海安226600 [2]海安市人民医院核医学科,江苏海安226600

出　　处：《生物技术》2023年第6期751-755,共5页Biotechnology

摘　　要：[目的]探究干扰素诱导T细胞α亚族/CXC趋化因子受体3(I-TAC/CXCR3)生物轴对甲状腺癌TPC-1细胞增殖、转移能力的影响。[方法]将体外培养的甲状腺癌细胞株TPC-1按处理方式不同分为对照组、I-TAC刺激组(100 ng/mL I-TAC)、I-TAC中和组(CXCR3中和抗体+100 ng/mL I-TAC)、CXCR3抑制组(15μg/mL CXCR3抑制剂AMG 487),RT-PCR、CCK-8、流式细胞术、Transwell实验、划痕实验、Western Blot检测各组细胞CXCR3 mRNA表达、细胞增殖、凋亡、侵袭、转移及I-TAC、CXCR3蛋白表达。[结果]与对照组比较,I-TAC刺激组CXCR3 mRNA表达(0.52±0.06 vs 0.91±0.02)、细胞增殖水平(1.13±0.17 vs 1.98±0.14)、穿膜细胞数(37.05±7.14 vs 57.41±9.62)、迁移距离(142.7±20.5 vs 376.2±31.9)增加,凋亡水平(5.52±0.73 vs 3.07±0.52)降低,CXCR3抑制组CXCR3 mRNA表达、细胞增殖水平、穿膜细胞数、迁移距离降低,凋亡水平升高(P<0.05);与I-TAC刺激组比较,I-TAC中和组CXCR3 mRNA表达(0.91±0.02 vs 0.49±0.05)、细胞增殖水平(1.98±0.14 vs 1.67±0.19)、穿膜细胞数(57.41±9.62 vs 32.93±6.58)、迁移距离(376.2±31.9 vs 143.6±21.3)降低,凋亡水平升高(3.07±0.52 vs 5.44±0.82,P<0.05)。[结论]I-TAC/CXCR3生物轴激活可促进甲状腺癌细胞的增殖、侵袭和转移,抑制其凋亡,阻断I-TAC/CXCR3生物轴相互作用或许能成为治疗甲状腺癌的新方法。[Objective]To study the impact of interferon-inducible T cell alpha-chemoattractant subfamily/CXC chemokine receptor 3(I-TAC/CXCR3)biological axis on the proliferation and metastasis of thyroid carcinoma TPC-1 cells.[Method]Thyroid carcinoma cell line TPC-1 cultured in vitro was divided into a control group,an I-TAC stimulation group(100 ng/mL I-TAC),an I-TAC neutralization group(CXCR3 neutralizing antibody+100 ng/mL I-TAC)and a CXCR3 inhibition group(15μg/mL CXCR3 inhibitor AMG 487)according to different treatment methods.CXCR3 mRNA expression,levels of cell proliferation,apoptosis,invasion,and metastasis as well as I-TAC and CXCR3 protein expression were detected by RT-PCR,CCK-8 assay,flow cytometer,transwell assay,scratch assay,and Western Blot.[Result]CXCR3 mRNA expression(0.52±0.06 vs 0.91±0.02),cell proliferation level(1.13±0.17 vs 1.98±0.14),number of penetrating cells(37.05±7.14 vs 57.41±9.62),and migration distance(142.7±20.5 vs 376.2±31.9)were increased and levels of apoptosis(5.52±0.73 vs 3.07±0.52)were lowered in the I-TAC stimulation group versus the control group,and CXCR3 mRNA expression,cell proliferation level,number of penetrating cells,and migration distance were decreased and levels of apoptosis were improved in the CXCR3 inhibition group versus the control group(P<0.05).Compared with the I-TAC stimulation group,CXCR3 mRNA expression(0.91±0.02 vs 0.49±0.05),cell proliferation level(1.98±0.14 vs 1.67±0.19),number of penetrating cells(57.41±9.62 vs 32.93±6.58),and migration distance(376.2±31.9 vs 143.6±21.3)were decreased and levels of apoptosis(3.07±0.52 vs 5.44±0.82)were improved in the I-TAC neutralization group(P<0.05).[Conclusion]Activation of I-TAC/CXCR3 biological axis can promote the proliferation,invasion and metastasis of thyroid carcinoma cells,inhibition the apoptosis,and blocking the effect of I-TAC/CXCR3 may be a new method for the treatment of thyroid carcinoma.

关 键 词：趋化因子配体人干扰素诱导T细胞α亚族 CXC趋化因子受体3 甲状腺癌 病理生物学行为 

分 类 号：R736.1[医药卫生—肿瘤]