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A comparative proteomic analysis for capsaicin‐induced apoptosis between human hepatocarcinoma (HepG2) and human neuroblastoma (SK‐N‐SH) cells
Author(s) -
Baek Yu Mi,
Hwang Hye Jin,
Kim Sang Woo,
Hwang Hee Sun,
Lee Sung Hak,
Kim Jung Ae,
Yun Jong Won
Publication year - 2008
Publication title -
proteomics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.26
H-Index - 167
eISSN - 1615-9861
pISSN - 1615-9853
DOI - 10.1002/pmic.200800094
Subject(s) - peroxiredoxin , oxidative stress , apoptosis , downregulation and upregulation , reactive oxygen species , catalase , sod2 , capsaicin , antioxidant , chemistry , gclm , microbiology and biotechnology , biology , superoxide dismutase , biochemistry , enzyme , receptor , gene , peroxidase , gclc
The endogenous ROS levels were increased during HepG2 apoptosis, whereas they were decreased during SK‐N‐SH apoptosis in response to capsaicin treatments. We used 2‐DE‐based proteomics to analyze the altered protein levels in both cells, with special attention on oxidative stress proteins before and after capsaicin treatments. The 2‐DE analysis demonstrated that 23 proteins were increased and 26 proteins were decreased significantly (fold change>1.4) in capsaicin‐treated apoptotic HepG2 and SK‐N‐SH cells, respectively. The distinct effect of capsaicin‐induced apoptosis on the expression pattern of HepG2 proteins includes the downregulation of some antioxidant enzymes including aldose reductase (AR), catalase, enolase 1, peroxiredoxin 1, but upregulation of peroxiredoxin 6, cytochrome c oxidase, and SOD2. In contrast, most antioxidant enzymes were increased in SK‐N‐SH cells in response to capsaicin, where catalase might play a pivotal role in maintenance of low ROS levels in the course of apoptosis. The global gene expression for oxidative stress and antioxidant defense genes revealed that 84 gene expressions were not significantly different in HepG2 cells between control and capsaicin‐treated cells. In contrast, a number of oxidative genes were downregulated in SK‐N‐SH cells, supporting the evidence of low ROS environment in apoptotic SK‐N‐SH cells after capsaicin treatment. It was concluded that the different relationship between endogenous ROS levels and apoptosis of two cancer cells presumably resulted from complicated expression patterns of many oxidative stress and antioxidant genes, rather than the individual role of some classical antioxidant enzymes such as SOD and catalase.