趋化因子fractalkine对裸鼠胰腺癌移植瘤生物学活性的影响  

Effect of Chemokine Fractalkine on the Growth of Tumors of Nude Mouse Model of Human Pancreatic Cancer

作　　者：史晓斌 黄李雅[2] SHI Xiaobin;HUANG Liya(Ningxia Medical University,Yinchuan 750004,China;Department of Gastroenterology,the General Hospital of Ningxia Medical University,Yinchuan 750004,China)

机构地区：[1]宁夏医科大学,银川750004 [2]宁夏医科大学总医院消化内科,银川750004

出　　处：《宁夏医科大学学报》2019年第2期147-151,共5页Journal of Ningxia Medical University

基　　金：国家自然科学基金(81460367);宁夏科学基金(2018AAC03161)

摘　　要：目的探讨趋化因子fractalkine(FKN)通过JAK2/STAT3信号通路对胰腺癌裸鼠皮下移植瘤生物学活性的影响。方法培养人胰腺癌细胞株PANC-1,以慢病毒为载体构建FKN-siRNA,建立裸鼠胰腺癌皮下肿瘤模型,观察肿瘤生长情况。试验分为对照组、FKN-siRNA阴性组(即只含有病毒载体组)和FKN-siRNA组,采用Western blot法检测各组肿瘤中FKN、JAK2、p-JAK2、STAT3及p-STAT3蛋白的表达。RT-qPCR法检测各组中FKN、JAK2和STAT3 mRNA的表达。结果 FKN-siRNA组肿瘤平均体积和质量均低于对照组和FKNsiRNA阴性组(P均<0.05)。Western blot检测结果显示,与对照组和FKN-siRNA阴性组相比,FKN-siRNA组FKN、JAK2、p-JAK2及p-STAT3蛋白表达量下降(P均<0.05)。RT-qPCR法检测结果,FKN-siRNA组FKN、JAK2及STAT3 mRNA的相对表达量较对照组和FKN-siRNA阴性组下降(P均<0.05)。结论 FKN可能是通过调控JAK2/STAT3信号通路促进胰腺癌生长。Objective To investigate the effect of fractalkine(FKN)on the biological activity of subcutaneous transplanted pancreatic cancer in nude mice through JAK2/STAT3 signaling pathway.Methods Human pancreatic cancer cell line PANC-1 was cultured,and FKN-siRNA was constructed with lentivirus as vector.The subcutaneous tumor model of pancreatic cancer in nude mice was established to observe the growth of tumor.The experiment was divided into control group,FKN-siRNA negative group(containing only viral vectors)and FKN-siRNA group.The expression of FKN,JAK2,p-JAK2,STAT3 and p-STAT3 protein was detected by Western blot.The expressions of FKN,JAK2 and STAT3 mRNA were detected by RT-qPCR.Results The average volume and mass of the tumors in the FKN-siRNA group were lower than those in the control group and the FKN-siRNA negative group(P<0.05).Western blot results showed that the expression of FKN,JAK2,p-JAK2 and p-STAT3 protein in the FKN-siRNA group decreased compared with the control group and the FKN-siRNA negative group(all P<0.05).The relative expression of FKN,JAK2 and STAT3 in FKN-siRNA group was significantly lower than that in control group and FKN-siRNA negative group(P<0.05).Conclusion FKN can promote the growth of pancreatic cancer,the mechanismmight be related to activation of JAK2/STAT3 pathway.

关 键 词：胰腺癌 趋化因子FRACTALKINE JAK2/STAT3通路 人胰腺癌细胞株PANC-1 SPF级BALB/C裸鼠 

分 类 号：R576[医药卫生—消化系统]