The Maillard reaction products are known to be effective in chemoprevention. Here, we focused on the anti-cancer effects of (E)-2,4-bis(p-hydroxyphenyl)-2-butenal on in vitro and in vivo colon cancer. We analysed the anti-cancer activity of (E)-2,4-bis(p-hydroxyphenyl)-2- butenal on colon cancer cells by using cell cycle and apoptosis analysis. To elucidate it's mechanism, NF-jB DNA binding activity, docking model as well as pull-down assay. Further, a xenograft model of colon cancer was studied to test the in vivo effects of (E)-2,4-bis(phydroxyphenyl)- 2-butenal. (E)-2,4-Bis(p- hydroxyphenyl)- 2-butenal inhibited colon cancer cells (SW620 and HCT116) growth followed by induction of apoptosis in a concentration-dependent manner via down-regulation of NF-jB activity. In docking model as well as pull-down assay, (E)-2,4-bis(p-hydroxyphenyl)-2-butenal directly binds to three amino acid residues of IKKb, thereby inhibited IKKb activity in addition to induction of death receptor 6 (DR6) as well as their target apoptotic genes. Finally, (E)-2,4-bis(p-hydroxyphenyl)-2-butenal suppressed anchorage-independent cancer cell growth, and tumor growth in xenograft model accompanied with apoptosis through inhibition of IKKb/NF-jB activity, and overexpression of DR6. These results suggest that (E)-2,4- bis(p-hydroxyphenyl)-2-butenal inhibits colon cancer cell growth through inhibition of IKKb/NF-jB activity and induction of DR6 expression. © Springer Science+Business Media New York 2013.
CITATION STYLE
Ban, J. O., Jung, Y. S., Kim, D. H., Park, K. R., Yun, H. M., Lee, N. J., … Hong, J. T. (2014). (E)-2,4-Bis(p-hydroxyphenyl)-2-butenal inhibits tumor growth via suppression of NF-jB and induction of death receptor 6. Apoptosis, 19(1), 165–178. https://doi.org/10.1007/s10495-013-0903-x
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