电离辐射通过转化生长因子-β-介导的上皮-间质转换来促进骨髓的侵袭迁移

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.

参考资料 ：阐释紫外光应该可通过转化介素-β（TGF-β）-内源性的上皮-内生转成 (EMT)来促进癌终点站粒体的侵袭移入。用到总和2Gy(60)Coγ终点站照射源自人类器官的6种癌终点站粒体，记录与EMT相关的变化，这包括分别利用显微镜新科技，蛋白质质索科利夫卡方法，免疫荧光新科技，样测试和Transwell泽田测试来通过观察并检测终点站粒体组织形态，EMT标明，侵袭移入能够等。采用蛋白质六轮免疫吸附法检测这些癌终点站粒体中TGF-β蛋白质水平，利用特别抑制剂SB431542来评估TGF-β讯号通路在紫外光EMT中的主导作用。经过总和为2Gy照射的癌终点站粒体中存在间叶终点站粒体的表达，与所谓照射组相对于其上皮标明减少，间叶终点站粒体标明增加，同时其侵袭分散能够大幅提高，TGF-β蛋白质水平也大幅提高。全面性找到由A549紫外光诱导的EMT可通过对TGF-β讯号抑制牵涉到逆转。这些结果显示TGF-β内源性的EMT在紫外光诱导大幅提高癌终点站粒体侵袭分散能够中起着关键主导作用。

出版人： lizexiu