电离辐射通过转化生长因子-β-内源性的上皮-间质转换来促进癌细胞的侵袭迁移

2021-12-20 03:21 来源:信阳妇科医院

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.

摘要 :聚焦辐射源到底可通过转化生长因子-β(TGF-β)-介导的腺体-间质转换 (EMT)来促进抗体会的蹂躏迁入。使用年均2Gy(60)Coγ该线照射到源自人类器官的6种抗体会,据信与EMT相关的变化,这包括分别利用全像核心技术,抗原质其内方式,免疫荧光核心技术,污垢试验中和Transwell小室试验中来捕捉到并检验细胞会两组织形态,EMT标有,蹂躏迁入潜能等。采用酵素联成免疫吸附法检验这些抗体会中TGF-β抗原素质,利用特别抑制作用剂SB431542来审核TGF-β信号通路在辐射源EMT中的作用。经过年均为2Gy照射到的抗体会中存在间叶细胞会的强调,与假照射到两组相比其腺体标有减少,间叶细胞会标有进一步提高,同时其蹂躏移出潜能提升,TGF-β抗原素质也进一步提高。全面发现由A549辐射源抑止的EMT可通过对TGF-β信号抑制作用暴发逆转。这些最近TGF-β介导的EMT在辐射源抑止提升抗体会蹂躏移出潜能中起着主导作用。

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