The enhancement of radiosensitivity in human esophageal carcinoma cells by thalidomide and its potential mechanism.

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Citation

Yu J, Liu F, Sun Z, Sun M, Sun S

The enhancement of radiosensitivity in human esophageal carcinoma cells by thalidomide and its potential mechanism.

Cancer Biother Radiopharm. 2011 Apr;26(2):219-27. doi: 10.1089/cbr.2010.0897.

PubMed ID
21539454 [ View in PubMed
]
Abstract

To investigate the effects of thalidomide on the radiosensitivity of human esophageal cancer cells (TE1 cells) and the potential mechanism underlying these effects. The effects of thalidomide on proliferation of TE1 cells were determined by Methyl thiazolyl tetrazolium assay. The multitarget click model was used to delineate the survival curve using a colony-forming assay, and the radiosensitivity was determined after TE1 cells were treated by thalidomide and/or X-ray radiation. The cell cycle was detected using flow cytometry. Our results are as follows: thalidomide alone suppressed the proliferation of TE1 cells in a dose- and time-dependent manner. The suppressive effects were enhanced by prolonged duration or elevated concentration of thalidomide. However, thalidomide did not affect the cell cycle of TE1 cells. The expression of vascular endothelial growth factor (VEGF) mRNA and protein was suppressed after treatment with thalidomide alone in a dose-dependent manner. Synergistic suppressive effects on VEGF expression were observed after administration of thalidomide and X-ray exposure. In conclusion, thalidomide was able to enhance the radiosensitivity of TE1 cells in vitro, which could be closely related to its suppressive effects on the expression of VEGF in TE1 cells, but had no obvious effects on the cell cycle.