电离辐射通过转化生长因子-β-酪氨酸的上皮-间质转换来促进癌细胞的侵袭迁移

2022-02-14 08:56 来源:濮阳妇科医院

Int J Radiat Oncol Biol Phys 2011 Dec;81 (5): 1530-7. [IF:4.503]Ionizing radiation promotes migration and invasion of cancer cells through transforming growth factor-Beta-mediated epithelial-mesenchymal transition.Zhou YC , Liu JY , Li J , Zhang J , Xu YQ , Zhang HW , Qiu LB , Ding GR , Su XM , Mei-Shi , Guo GZ .Department of Radiation Oncology, Xijing Hospital Fourth Military Medical University, Xi'an, China; Department of Radiation Medicine, College of Preventive Medicine, Xijing Hospital Fourth Military Medical University, Xi'an, China.第四军医大学西京医院放射科

AbstractTo examine whether ionizing radiation enhances the migratory and invasive abilities of cancer cells through transforming growth factor (TGF-β)-mediated epithelial-mesenchymal transition (EMT). Six cancer cell lines originating from different human organs were irradiated by (60)Co γ-ray at a total dose of 2 Gy, and the changes associated with EMT, including morphology, EMT markers, migration and invasion, were observed by microscope, Western blot, immunofluorescence, scratch assay, and transwell chamber assay, respectively. Then the protein levels of TGF-β in these cancer cells were detected by enzyme-linked immunosorbent assay, and the role of TGF-β signaling pathway in the effect of ionizing radiation on EMT was investigate by using the specific inhibitor SB431542. After irradiation with γ-ray at a total dose of 2 Gy, cancer cells presented the mesenchymal phenotype, and compared with the sham-irradiation group the expression of epithelial markers was decreased and of mesenchymal markers was increased, the migratory and invasive capabilities were strengthened, and the protein levels of TGF-β were enhanced. Furthermore, events associated with EMT induced by IR in A549 could be reversed through inhibition of TGF-β signaling. These results suggest that EMT mediated by TGF-β plays a critical role in IR-induced enhancing of migratory and invasive capabilities in cancer cells.

概述 :探讨放射是否可通过转换成酪氨酸-β(TGF-β)-内源性的视网膜-上皮转换 (EMT)来有利于细胞内的摧残搬迁。使用总量2Gy(60)Coγ本站反射来源于人类器官的6种细胞内,据信与EMT相关的变化,这包括分别并用显微镜核心技术,蛋白质印迹方法,免疫荧光核心技术,污垢试验和Transwell四人试验来通过观察并扫描细胞内组织形态,EMT标记,摧残搬迁潜能等。采用复合物联免疫吸附法扫描这些细胞内中的TGF-β蛋白水准,并用特别抑制作用SB431542来检验TGF-β信号通道在放射EMT中的的作用。经过总量为2Gy反射的细胞内中的存在间叶细胞内的表达,与假反射组相比其视网膜标记减少,间叶细胞内标记增加,同时其摧残分散潜能减慢,TGF-β蛋白水准也提升。进一步辨认出由A549放射抑止的EMT可通过对TGF-β信号抑制作用起因再一。这些结果表明TGF-β内源性的EMT在放射抑止减慢细胞内摧残分散潜能中的起着关键作用。

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