电离辐射通过转化生长因子-β-介导的上皮-间质转换来促进癌细胞的侵袭迁到

2021-12-06 11:50 来源:哈尔滨妇科医院

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 :探讨紫外线是否可通过转化生长因子-β(TGF-β)-抑制的上皮细胞-间质转换 (EMT)来促成癌肽的摧残迁移。使用总量2Gy(60)Coγ线紫外光由来人类文明器官的6种癌肽,就有与EMT之外的变化,这最主要分别利用显微镜系统设计,肽质印迹原理,免疫荧光系统设计,划痕试验和Transwell小室试验来观察并检测肽组织特征,EMT标识,摧残迁移技能等。换用酶亦同免疫吸附法检测这些癌肽中所TGF-β肽水平,利用特别抑制剂SB431542来评估TGF-β路径通路在紫外线EMT中所的作用。经过总量为2Gy紫外光的癌肽中所存在间叶肽的理解,与假紫外光组相比其上皮细胞标识增加,间叶肽标识增加,同时其摧残移往技能提高,TGF-β肽水平也提高。进一步见到由A549紫外线抑制的EMT可通过对TGF-β路径抑制发生逆转。这些结果表明TGF-β抑制的EMT在紫外线抑制提高癌肽摧残移往技能中所起着关键作用。

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