电离辐射通过升华生长因子-β-介导的上皮-间质转换来促进癌细胞的侵袭迁移

2021-12-06 01:39 来源:西宁妇科医院

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 :探讨远红外线应该可通过转化生长因子-β(TGF-β)-介导的上皮-间质反转 (EMT)来促进癌氨基酸的波及移往。可用总量2Gy(60)Coγ线反射源自人类文明器官的6种癌氨基酸,据信与EMT相关的巨大变化,这包括分别透过显微镜技术,氨基酸斯塔夫基方规,免疫荧光技术,划痕测试和Transwell小室测试来仔细观察并样品氨基酸组织形态,EMT标有,波及移往控制能力等。采用酶联免疫吸附规样品这些癌氨基酸之前TGF-β抗原水平,透过特别胺SB431542来评估TGF-β信号通路在远红外线EMT之前的作用。经过总量为2Gy反射的癌氨基酸之前实际上间叶氨基酸的表达,与实为反射组相比其上皮标有减少,间叶氨基酸标有提高,同时其波及集中于控制能力增强,TGF-β抗原水平也提高。有利于推测由A549远红外线正向的EMT可通过对TGF-β信号抑制发生逆转。这些结果表明TGF-β介导的EMT在远红外线正向增强癌氨基酸波及集中于控制能力之前起着关键作用。

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