QI Ya-li,WANG Jun,LI Yan,et al.Effect of ionizing radiation combined with inhibitors or inducer of autophagy and apoptosis on MCF7 cells[J].Chinese Journal of Radiological Medicine and Protection,2010,30(3):263-266 |
Effect of ionizing radiation combined with inhibitors or inducer of autophagy and apoptosis on MCF7 cells |
Received:August 20, 2009 |
DOI:10.3760/cma.j.issn.0254-5098.2010.03.008 |
KeyWords:Ionizing radiation Autophagy Apoptosis Inductor Inhibitor |
FundProject:国家自然科学基金(30970681) |
|
Hits: 4452 |
Download times: 2238 |
Abstract:: |
Objective To detect the inhibiting effects of ionizing radiation combined with inhibitors or inducer of autophagy and apoptosis on MCF7 cell line, and to provide the evidence for human breast cancer therapy radiation.Methods MCF7 cells were exposed to X-rays and randomly divided into 4 groups, including 0 Gy, 4 Gy, 4 Gy+rapamycin, 4 Gy+ 3-MA, and 4 Gy+z-VAD-fmk groups, respectively. The growth doubling time was calculated by MTT method. The specific protein expressions of LC3 autophagy and beclin1 were detected by using Western blot and the difference of protein contents was compared. The percentage of apoptosis of MCF7 cells was measured by flow cytometry (FCM). Results The growth doubling time of MCF7 cells in 4 Gy group was longer than that in 0 Gy group (t= 4.41,P<0.05), but shorter than that in 4 Gy + rapamycin group (t= 4.35,P<0.05). Compared to 4 Gy + rapamycin group, both of the growth doubling time in 4 Gy + 3-MA and 4 Gy + z-VAD-fmk groups were shorter (t= 4.32, P<0.05). The expressions of beclin1 and LC3-Ⅱ proteins in 4 Gy+rapamycin group were the highest, while those in 4 Gy+3-MA group the lowest. Except for 4 Gy + 3-MA and 4 Gy + z-VAD-fmk groups, there were significant differences among the other groups in two protein expressions (t= 3.91-4.78,P<0.05).Conclusions Ionizing radiation could induce MCF7 cell autophagy, promote the apoptosis of tumor cells in combination with autophagy inducer. Ionizing radiation combined with autophagy inhibitor might inhibit the development of autophagy, and delay the apoptosis of tumor cells. |
HTML View Full Text View/Add Comment Download reader |
Close |
|
|
|