(E)-2,4-Bis(p-hydroxyphenyl)-2-butenal inhibits tumor growth via suppression of NF-jB and induction of death receptor 6

Jung Ok Ban; Young Suk Jung; Dae Hwan Kim; Kyung Ran Park; Hyung Mun Yun; Nam Jin Lee; Hee Pom Lee; Jeong Hyun Shim; Heon Sang Jeong; Yun Hee Lee; Young Wan Ham; Sang Bae Han; Jin Tae Hong

doi:10.1007/s10495-013-0903-x

(E)-2,4-Bis(p-hydroxyphenyl)-2-butenal inhibits tumor growth via suppression of NF-jB and induction of death receptor 6

Jung Ok Ban, Young Suk Jung, Dae Hwan Kim, Kyung Ran Park, Hyung Mun Yun, Nam Jin Lee, Hee Pom Lee, Jeong Hyun Shim, Heon Sang Jeong, Yun Hee Lee, Young Wan Ham, Sang Bae Han, Jin Tae Hong

Department of Pharmacy

Research output: Contribution to journal › Article › peer-review

14 Citations (Scopus)

Abstract

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.

Original language	English
Pages (from-to)	165-178
Number of pages	14
Journal	Apoptosis
Volume	19
Issue number	1
DOIs	https://doi.org/10.1007/s10495-013-0903-x
Publication status	Published - 2014 Jan

Bibliographical note

Funding Information:
Acknowledgments This work was supported by the National Research Foundation of Korea (NRF) Grant by the Korea government (MEST; MRC, 2012-0029480), and by the Ministry of Trade, Industry and Energy (MOTIE, 1415126993) through the fostering project of Osong Academy-Industry Convergence (BAIO).

All Science Journal Classification (ASJC) codes

Pharmacology
Pharmaceutical Science
Clinical Biochemistry
Cell Biology
Biochemistry, medical
Cancer Research

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1007/s10495-013-0903-x

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@article{897c4dd796474423be939406eb109cf5,

title = "(E)-2,4-Bis(p-hydroxyphenyl)-2-butenal inhibits tumor growth via suppression of NF-jB and induction of death receptor 6",

abstract = "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.",

author = "Ban, {Jung Ok} and Jung, {Young Suk} and Kim, {Dae Hwan} and Park, {Kyung Ran} and Yun, {Hyung Mun} and Lee, {Nam Jin} and Lee, {Hee Pom} and Shim, {Jeong Hyun} and Jeong, {Heon Sang} and Lee, {Yun Hee} and Ham, {Young Wan} and Han, {Sang Bae} and Hong, {Jin Tae}",

note = "Funding Information: Acknowledgments This work was supported by the National Research Foundation of Korea (NRF) Grant by the Korea government (MEST; MRC, 2012-0029480), and by the Ministry of Trade, Industry and Energy (MOTIE, 1415126993) through the fostering project of Osong Academy-Industry Convergence (BAIO).",

year = "2014",

month = jan,

doi = "10.1007/s10495-013-0903-x",

language = "English",

volume = "19",

pages = "165--178",

journal = "Apoptosis : an international journal on programmed cell death",

issn = "1360-8185",

publisher = "Springer Netherlands",

number = "1",

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T1 - (E)-2,4-Bis(p-hydroxyphenyl)-2-butenal inhibits tumor growth via suppression of NF-jB and induction of death receptor 6

AU - Ban, Jung Ok

AU - Jung, Young Suk

AU - Kim, Dae Hwan

AU - Park, Kyung Ran

AU - Yun, Hyung Mun

AU - Lee, Nam Jin

AU - Lee, Hee Pom

AU - Shim, Jeong Hyun

AU - Jeong, Heon Sang

AU - Lee, Yun Hee

AU - Ham, Young Wan

AU - Han, Sang Bae

AU - Hong, Jin Tae

N1 - Funding Information: Acknowledgments This work was supported by the National Research Foundation of Korea (NRF) Grant by the Korea government (MEST; MRC, 2012-0029480), and by the Ministry of Trade, Industry and Energy (MOTIE, 1415126993) through the fostering project of Osong Academy-Industry Convergence (BAIO).

PY - 2014/1

Y1 - 2014/1

N2 - 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.

AB - 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.

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(E)-2,4-Bis(p-hydroxyphenyl)-2-butenal inhibits tumor growth via suppression of NF-jB and induction of death receptor 6

Abstract

Bibliographical note

All Science Journal Classification (ASJC) codes

UN SDGs

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