摘要
目的:探讨JAK2/STAT3通路对胰腺癌SW1990细胞侵袭迁移能力的影响,研究肿瘤相关巨噬细胞(TAMs)促进胰腺癌演进的机制。方法:通过密度梯度离心法获取健康成人外周血单个核细胞,采用IL-4体外诱导选择性激活巨噬细胞(M2),模拟胰腺癌微环境中的TAMs,并将不同激活状态的巨噬细胞与胰腺癌SW1990细胞进行共培养。采用q-PCR和western blotting实验检测胰腺癌SW1990细胞JAK2、STAT3 m RNA与蛋白水平的变化,划痕实验和Transwell实验分别检测细胞迁移与侵袭能力的变化。结果:M2可明显上调胰腺癌SW1990细胞JAK2、STAT3的m RNA(P<0.05)与蛋白水平(P<0.05),共培养32 h后可显著促进胰腺癌SW1990细胞的横向迁移(P<0.05)和纵向侵袭能力(P<0.05)。结论:M2可通过JAK2/STAT3信号通路促进胰腺癌SW1990细胞的侵袭和迁移。
Objective: To investigate the effects of JAK2 / STAT3 signaling pathway on the invasion and migration of pancreatic cancer SW1990 cells, and study the specific mechanism of tumor-associated macrophages(TAMs) in promoting the tumorigenesis and progression of pancreatic cancer. Methods: Perip- heral blood mononuclear cells of healthy aduhs were isolated by means of density gradient centrifugation, alternatively-activated macrophages were induced by the stimulation of interleukin-4 in vitro, and pancreatic cancer SW1990 cells and macrophages were co-cultured with differentiate activated states in order to simulate TAMs in the pancreatic cancer microenvironment. The mRNA and protein levels of JAK2 and STAT3 were evaluated by real-time q-PCR and western blotting. The ability of migration and invasion was detected by wound healing assay and transwell chamber assay respectively. Results: The mRNA and protein levels of JAK2 and STAT3 were significantly in creased evaluated by qRT-PCR and westernblotting (P〈0.05). Wound healing assays and transwell chamber assays indicated that alternatively activated macrophages obviously promoted the migration and invasion of SW1990 cells after 32 h's co-culture (P〈 0.05). Conclusion: Alternatively-activated macrophages can promote the ability of migration and invasion of pancreatic cancer SW1990 cells via JAK2 / STAT3 signaling pathway.
出处
《华夏医学》
CAS
2016年第3期30-35,共6页
Acta Medicinae Sinica