scholarly journals Involvement of c-Myc in low dose radiation-induced senescence enhanced migration and invasion of unirradiated cancer cells

Aging ◽  
2021 ◽  
Author(s):  
Jyh-Der Leu ◽  
Chung-Yih Wang ◽  
Chia-Chien Lo ◽  
Min-Ying Lin ◽  
Chun-Yuan Chang ◽  
...  
2009 ◽  
Vol 172 (3) ◽  
pp. 306-313 ◽  
Author(s):  
Kelvin K. C. Tsai ◽  
Jeremy Stuart ◽  
Yao-Yu Eric Chuang ◽  
John B. Little ◽  
Zhi-Min Yuan

2013 ◽  
Vol 18 ◽  
pp. S179-S180 ◽  
Author(s):  
I. Alastuey ◽  
A. Noé ◽  
C. Chiaramello ◽  
S. Montemuiño ◽  
J. Pardo

2008 ◽  
Vol 2 ◽  
pp. CMO.S463
Author(s):  
Elizabeth K. Balcer-Kubiczek ◽  
Mona Attarpour ◽  
Jian Z. Wang ◽  
William F. Regine

Low-dose radiation hypersensitivity (HRS) describes a phenomenon of excessive sensitivity to X ray doses <0.5 Gy. Docetaxel is a taxane shown to arrest cells in the G2/M phase of the cell cycle. Some previous studies suggested that HRS might result from the abrogation of the early G2 checkpoint arrest. First we tested whether HRS occurs in gastric cancer—derived cells, and whether pre-treatment of cells with low docetaxel concentrations can enhance the magnitude of HRS in gastric cancer cells. The results demonstrated HRS at ~0.3 Gy and the synergy between 0.3 Gy and docetaxel (3 nM for 24 h), and the additivity of other drug/dose combinations. The synergistic effect was associated with a significant docetaxel-induced G2 accumulation. Next, we evaluated in time-course experiments ATM kinase activity and proteins associated with the induction and maintenance of the early G2 checkpoint. The results of multi-immunoblot analysis demonstrate that HRS does not correlate with the ATM-dependent early G2 checkpoint arrest. We speculate that G2 checkpoint adaptation, a phenomenon associated with a prolonged cell cycle arrest, might be involved in HRS. Our results also suggest a new approach for the improvement the effectiveness of docetaxel-based radiotherapy using low doses per fraction.


2009 ◽  
Vol 27 (15_suppl) ◽  
pp. e22113-e22113
Author(s):  
M. N. Jha ◽  
J. S. Bedford ◽  
S. Jha ◽  
K. Prasad

e22113 Background: It is estimated that low dose radiation can increase the risk of cancer as well as mutations. However, the interaction of low dose radiation with caffeine has not been adequately investigated. We investigated the effects of caffeine on low dose- gamma-radiation-induced chromosomal damage in human T leukemia cells (Jurket T-cells) and two normal human fibroblast cell lines (AG1522 and GM 2149). Method: Jurkat cells were maintained in RPMI 1640 medium and fibroblast in alpha-minimal essential medium (MEM) All cells were incubated at 37o C in a humidified atmosphere of 5% CO2 in air. Cells from the exponential phase were treated with 1 mg/ml caffeine ( control cells received same amount of solvent) and irradiated with low doses (3, 5, 10, 20 and 40 cGy,), using a 137 Cs-gamma radiation source. Colcemid at a concentration of 0.1 μg/ml was added to every flask. Cells were fixed in methanol: acetic acid solution and stained with Giemsa. 100 irradiated and un-irradiated metaphase- like cells were scored for chromatid-type aberrations. Results: Low dose gamma-radiation increased the levels of chromatid breaks(dose dependent) in both normal and cancer cells; however, cancer cells appeared to be more sensitive than the normal cells. Caffeine treatment markedly increased chromatid aberrations in Jurkat T-cells at all radiation doses but not in normal cells. Previously, we reported that caffeine eliminates gamma-ray-induced G2 delay in other human tumor cells but not normal cells (Jha, et.al., Radiat. Res. 157, 26–31, 2002). Conclusions: The mechanisms that may underlie this differential effect of caffeine in cancer and normal cells are unknown, but if one result of a G2 delay is to allow more time for chromosome breakage rejoining processes to occur, then elimination of this delay by caffeine in tumor cells but not normal cells might account for the difference. To the extent these observations are generally true for tumor vs normal cells, the differential sensitization could have an impact in improving the efficacy of radiation therapy. No significant financial relationships to disclose.


2014 ◽  
Vol 10 (3) ◽  
pp. 1569-1575 ◽  
Author(s):  
YONG XIN ◽  
HAI-BIN ZHANG ◽  
TIAN-YOU TANG ◽  
GUI-HONG LIU ◽  
JIAN-SHE WANG ◽  
...  

2010 ◽  
Vol 173 (2) ◽  
pp. 125-137 ◽  
Author(s):  
Benjamin J. Blyth ◽  
Edouard I. Azzam ◽  
Roger W. Howell ◽  
Rebecca J. Ormsby ◽  
Alexander H. Staudacher ◽  
...  

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