通过抑制巨噬细胞的趋化迁移，五聚体蛋白3沉默抑制胃癌相关炎症。
Pentraxin-3 Silencing Suppresses Gastric Cancer-related Inflammation by Inhibiting Chemotactic Migration of Macrophages.
作者信息
Choi Bongkun, Lee Eun-Jin, Park Young Soo, Kim Sang-Min, Kim Eun-Young, Song Youngsup, Kang Sang-Wook, Rhu Min-Hee, Chang Eun-Ju
机构信息
Department of Biomedical Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea Cell Dysfunction Research Center, University of Ulsan College of Medicine, Seoul, Republic of Korea.
Department of Pathology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea.
出版信息
Anticancer Res. 2015 May;35(5):2663-8.
BACKGROUND
Chronic inflammation characterized by the recruitment and activation of macrophages has been implicated in the development of gastric cancer.
MATERIALS AND METHODS
Expression of the long form of pentraxin-3 (PTX3) in gastric cancer cells was examined by reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay. The migratory capacity of gastric cancer cells and chemotaxis of macrophages by PTX3 were assessed by wound-healing and transwell assays. PTX3 silencing using small interfering RNA (siRNA) was performed to confirm PTX3-mediated effects.
RESULTS
We demonstrated that PTX3 expression was elevated in human advanced gastric cancer tissues with increased infiltration of CD11b+ macrophages. Tumor necrosis factor-alpha increased PTX3 expression via nuclear factor-kappa B activation in human gastric cancer cells. PTX3 promoted the tumor cell migratory potential, the recruitment of macrophages and their subsequent binding to gastric cancer cells. These effects were suppressed by PTX3 knockdown using siRNA.
CONCLUSION
Our findings suggest that gastric cancer-derived PTX3 promotes macrophage recruitment, which may contribute to gastric cancer-related inflammation.
背景
以巨噬细胞募集和激活为特征的慢性炎症与胃癌的发生发展有关。
材料与方法
采用逆转录-聚合酶链反应和酶联免疫吸附测定法检测胃癌细胞中长型五聚体3（PTX3）的表达。通过伤口愈合实验和Transwell实验评估PTX3对胃癌细胞迁移能力和巨噬细胞趋化性的影响。使用小干扰RNA（siRNA）沉默PTX3以证实PTX3介导的作用。
结果
我们证明，在人晚期胃癌组织中PTX3表达升高，且CD11b +巨噬细胞浸润增加。肿瘤坏死因子-α通过激活人胃癌细胞中的核因子-κB增加PTX3表达。PTX3促进肿瘤细胞迁移潜能、巨噬细胞募集及其随后与胃癌细胞的结合。使用siRNA敲低PTX3可抑制这些作用。
结论
我们的研究结果表明，胃癌来源的PTX3促进巨噬细胞募集，这可能导致与胃癌相关的炎症。
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