Aryl hydrocarbon receptor-dependent apoptotic cell death induced by the flavonoid chrysin in human colorectal cancer cells
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- 作者：Sean M. Ronnekleiv-Kelly ; Manabu Nukaya ; Carol J. Dí ; az-Dí ; az ; Bryant W. Megna ; Patrick R. Carney ; Peter G. Geiger ; Gregory D. Kennedy ; kennedyg@surgery.wisc.edu" class="auth_mail" title="E-mail the corresponding author
- 关键词：AHR ; aryl hydrocarbon receptor ; AP-1 ; activator protein 1 ; ARNT ; AHR nuclear translocator ; BAD ; Bcl-2-associated death promoter ; CYP ; cytochrome P450 ; DRE ; dioxin-responsive element ; ERK ; extracellular signal-regulated kinase ; FICZ ; 6-formylindolo (3 ; 2-b) carbazole ; IEGs ; immediate early genes ; JNK ; c-jun N-terminal kinase ; LTα ; lymphotoxin α ; MAPK ; mitogen-activated protein kinase ; NF-κB ; nuclear factor κ-light-chain enhancer of activated B cells ; PYCARD ; PYD and CARD domain containing ; rTdT ; r
- 刊名：Cancer Letters
- 出版年：2016
- 出版时间：1 January 2016
- 年：2016
- 卷：370
- 期：1
- 页码：91-99
- 全文大小：930 K
文摘
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The treatment of flavonoid chrysin showed a chemopreventive effect in human colorectal cancer cells via the apoptosis pathway.
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Up-regulation and activation of the tumor necrosis factor-mediated transcriptional pathway were involved in apoptosis.
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The aryl hydrocarbon receptor, a ligand-receptor for chrysin, is required for the induction of apoptosis.