电离辐射通过转化生长因子-β-介导的上皮-间质转换成来促进癌细胞的侵袭迁移

2022-01-03 06:09 来源:西安妇科医院

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.

概要 :探讨强磁场是否可通过转化生长因子-β(TGF-β)-介导的黏膜-内生转换 (EMT)来促进肝细胞的波及迁移。用作总和2Gy(60)Coγ线光照意指人类器官的6种肝细胞,记录与EMT相关的变化,这最主要分别借助显微镜应用,蛋白质质印迹方法,免疫荧光应用,凹凸试验和Transwell小室试验来捕捉到并检测肝细胞第一组织共通点,EMT标上,波及迁移能力等。采用酶联免疫吸附法检测这些肝细胞之前TGF-β蛋白质低水平,借助尤其胺SB431542来审计TGF-β信号通路在强磁场EMT之前的作用。经过总和为2Gy光照的肝细胞之前存在间叶肝细胞的表达,与假光照第一组相比其黏膜标上减小,间叶肝细胞标上增加,同时其波及转移能力加强,TGF-β蛋白质低水平也大幅提高。再进一步发现由A549强磁场抑止的EMT可通过对TGF-β信号抑制时有发生逆转。这些得出TGF-β介导的EMT在强磁场抑止加强肝细胞波及转移能力之前起着关键作用。

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