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Radio-induced modulation of transforming growth factor β1 sensitivity in a p53 wild-type human colorectal-cancer cell line

✍ Scribed by Laurent Suardet; Chuan Li; John B. Little

Publisher
John Wiley and Sons
Year
1996
Tongue
French
Weight
654 KB
Volume
68
Category
Article
ISSN
0020-7136

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✦ Synopsis

Unlike normal intestinal cells, colorectal-carcinoma cell lines are usually not responsive to transforming growth factor PI. The cyclin-dependent kinase inhibitor p2 I that is induced by X irradiation in cells expressing normal pS3 can also be induced by TCF-P I by a p53-independent pathway. We have investigated possible interactions between ionizing radiation and TCF-P I, using a panel of 8 human colorectal-cancer cell lines varying in p53 status and sensitivity to the cyto-inhibitory effect of TGF-P I. Heterogeneity in the radiosensitivity of these cell lines was observed, with SFz (surviving fraction after irradiation with 2 Cy) ranging from 0.19 to 0.82. Radioresistance (high SFz values) was in general associated with abnormal expression of p53. An effect of TGF-PI treatment on radiosensitivity was observed with one cell line only (LS5 13). and manifested by enhancement of the qtotoxic effect of radiation. In an experiment with fractionated irradiation during continuous exposure to TGF-P I, there was no change in the intrinsic radiosensitivity of LS5 I 3 cells, though irradiated cells treated with TGF-PI were more sensitive to the first radiation dose. Irradiated LS5 I3 colorectalcancer and Mv-I-Lu epithelial cells were significantly more sensitive to TCF-PI than were unimtdiated controls, whereas no change was observed in the TGF-P I sensitivity of irradiated LS I034 cells. Radio-induced modulation of TCF-P I sensitivity was transitory and declined before the decline to baseline level of pZl mRNA expression. On the basis of these results, we postulate that radiation-induced sensitization to TGF-P I occurs in TCF-P I-sensitive cells expressing wild-type p53.

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