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6‐Shogaol induces apoptosis in human colorectal carcinoma cells via ROS production, caspase activation, and GADD 153 expression
Author(s) -
Pan MinHsiung,
Hsieh MinChi,
Kuo JenMin,
Lai ChingShu,
Wu Hou,
Sang Shengmin,
Ho ChiTang
Publication year - 2008
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.200700157
Subject(s) - apoptosis , reactive oxygen species , cytochrome c , dna fragmentation , microbiology and biotechnology , biology , chemistry , programmed cell death , biochemistry
Ginger, the rhizome of Zingiber officinale , is a traditional medicine with anti‐inflammatory and anticarcinogenic properties. This study examined the growth inhibitory effects of the structurally related compounds 6‐gingerol and 6‐shogaol on human cancer cells. 6‐Shogaol [1‐(4‐hydroxy‐3‐methoxyphenyl)‐4‐decen‐3‐one] inhibits the growth of human cancer cells and induces apoptosis in COLO 205 cells through modulation of mitochondrial functions regulated by reactive oxygen species (ROS). ROS generation occurs in the early stages of 6‐shogaol‐induced apoptosis, preceding cytochrome c release, caspase activation, and DNA fragmentation. Up‐regulation of Bax, Fas, and FasL, as well as down‐regulation of Bcl‐2 and Bcl‐X L were observed in 6‐shogaol‐treated COLO 205 cells. N ‐acetylcysteine (NAC), but not by other antioxidants, suppress 6‐shogaol‐induced apoptosis. The growth arrest and DNA damage (GADD)‐inducible transcription factor 153 (GADD153) mRNA and protein is markedly induced in a time‐ and concentration‐dependent manner in response to 6‐shogaol.