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DAPK1 modulates a curcumin-induced G2/M arrest and apoptosis by regulating STAT3, NF-κB, and caspase-3 activation
- Wu, Bingshan, Yao, Hui, Wang, Shanshan, Xu, Ruxiang
- Biochemical and biophysical research communications 2013 v.434 pp. 75-80
- Curcuma longa, anticarcinogenic activity, apoptosis, caspase-3, cell cycle, curcumin, death, gene expression, messenger RNA, neoplasm cells, protein kinases, therapeutics, transcription factor NF-kappa B
- Curcumin, an active polyphenol extracted from the perennial herb Curcuma longa, controls various molecules involved in tumor cell death. In this study, we found that the tumor suppressor death-associated protein kinase 1 (DAPK1) plays a vital role in the anti-carcinogenic effects of curcumin. We found that curcumin increased DAPK1 expression at the mRNA and protein levels in U251 cells, and that the siRNA-mediated knockdown of DAPK1 attenuated the curcumin-induced inhibition of STAT3 and NF-κB. Moreover, DAPK1 suppression diminished curcumin-induced caspase-3 activation. In addition, we confirmed that DAPK1 was required for a curcumin-induced G2/M cell cycle arrest and apoptosis. Thus, DAPK1 is involved in curcumin-mediated death pathways. Our data suggest novel mechanisms for curcumin in cancer therapy.