Abrogation of G2/M arrest sensitizes curcumin-resistant hepatoma cells to apoptosis

Key Laboratory of Gene Engineering of the Ministry of Education, School of Life Sciences, Sun Yat-Sen University, Xin Gang Xi Road 135, Guangzhou 510275, PR China.
FEBS Letters (Impact Factor: 3.34). 08/2008; 582(18):2689-95. DOI: 10.1016/j.febslet.2008.06.048
Source: PubMed

ABSTRACT In this study, we showed that curcumin treatment resulted in activation of Chk1-mediated G2 checkpoint, which was associated with the induction of G2/M arrest and the resistance of cancer cells to curcumin-induced apoptosis. Further investigation revealed that inhibition of Chk1 significantly abrogated G2/M arrest and sensitized curcumin-resistant cells to apoptosis via upregulation of Bad and in turn the loss of mitochondrial membrane potential. These results indicate that Chk1-mediated G2/M arrest may serve as a mechanism for curcumin resistance and Chk1 represents a potential target for the reversal of this resistance. Our findings should be helpful for clinical application of curcumin.

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Available from: Jiasen Cheng, Aug 06, 2015
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    • "Those processes are usually associated with G2/M arrest [58] [59]. On the other hand there is evidence in breast cancer that 14-3-3σ upregulation is correlated with drug resistance [60] and that abrogation of G2/M arrest may augment the effects of anticancer treatment [61], especially irradiation [62] [63]. In EC cell lines, G2/M arrest induced by DAC was tightly correlated with inhibition of cell proliferation. "
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