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提高大鼠208F成纤维细胞系对辐射诱导凋亡的敏感性并不会改变其克隆形成存活剂量反应。

Increasing the susceptibility of the rat 208F fibroblast cell line to radiation-induced apoptosis does not alter its clonogenic survival dose-response.

作者信息

Aldridge D R, Arends M J, Radford I R

机构信息

Research Division, Peter MacCallum Cancer Institute, Melbourne, Australia.

出版信息

Br J Cancer. 1995 Mar;71(3):571-7. doi: 10.1038/bjc.1995.111.

Abstract

Recent studies have suggested a correlation between the rate and incidence of apoptosis and the radiation response of particular cell lines. However, we found that increasing the rate of induction of apoptosis in the fibroblast line 208F, by transfecting it with human c-myc, did not lead to a change in its clonogenic survival dose-response for either gamma-irradiation or 125I-induced DNA damage. It was also found that expression of mutant (T24) Ha-ras in the 208F line appeared to decrease the level of apoptosis per mitosis after irradiation and inhibited the formation of nucleosomal ladders, but did not affect either the onset of the morphological features of apoptosis or the clonogenic survival dose-response of the cells to either gamma-irradiation or 125I-induced DNA damage. Our findings suggest that it may be incorrect to make predictions about the radiosensitivity of cells based only on knowledge of their mode of death.

摘要

最近的研究表明,特定细胞系的凋亡速率和发生率与辐射反应之间存在相关性。然而,我们发现,通过用人c-myc转染成纤维细胞系208F来提高其凋亡诱导速率,并未导致其对γ射线照射或¹²⁵I诱导的DNA损伤的克隆形成存活剂量反应发生变化。还发现,在208F细胞系中突变型(T24)Ha-ras的表达似乎降低了照射后每个有丝分裂期的凋亡水平,并抑制了核小体梯带的形成,但既不影响凋亡形态特征的出现,也不影响细胞对γ射线照射或¹²⁵I诱导的DNA损伤的克隆形成存活剂量反应。我们的研究结果表明,仅根据细胞死亡模式的知识来预测细胞的放射敏感性可能是不正确的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72d3/2033634/9723765531fe/brjcancer00049-0147-a.jpg

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