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Resveratrol Affects Protein Kinase C Activity and Promotes Apoptosis in Human Colon Carcinoma Cells
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  • Resveratrol Affects Protein Kinase C Activity and Promotes Apoptosis in Human Colon Carcinoma Cells
  • Resveratrol Affects Protein Kinase C Activity and Promotes Apoptosis in Human Colon Carcinoma Cells
저자명
Fang. Jie-Yu,Li. Zhi-Hua,Li. Qiang,Huang. Wen-Sheng,Kang. Liang,Wang. Jian-Ping
간행물명
Asian Pacific journal of cancer prevention : APJCP
권/호정보
2012년|13권 12호|pp.6017-6022 (6 pages)
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아시아태평양암예방학회
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정기간행물|ENG|
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이 논문은 한국과학기술정보연구원과 논문 연계를 통해 무료로 제공되는 원문입니다.
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Background: Resveratrol has been reported to have potential chemopreventive and apoptosis-inducing properties in a variety of tumor cell lines. Objective: In this study, to investigate the effects of resveratrol on protein kinase C (PKC) activity and apoptosis in human colon carcinoma cells, we used HT-29 cells and examined the $PKC{alpha}$ and ERK1/2 signaling pathways. Methods: To test the effects of resveratrol on the growth of HT-29 cells, the cells were exposed to varying concentrations and assessed with the the MTT cell-viability assay. Fluorescence-activated cell sorter (FACS) analysis was applieded to determine the effects of resveratrol on cell apoptosis. Western blotting was performed to determine the protein levels of $PKC{alpha}$ and ERK1/2. In inhibition experiments, HT-29 cells were treated with G$ddot{o}$6976 or PD98059 for 30 min, followed by exposure to $200{mu}M$ resveratrol for 72 h. Results: Resveratrol had a significant inhibitory effect on HT-29 cell growth. FACS revealed that resveratrol induced apoptosis. Western blotting showed that e phosphorylation of $PKC{alpha}$ and ERK1/2 was significantly increased in response to resveratrol treatment. Pre-treatment with $PKC{alpha}$ and ERK1/2 inhibitors (G$ddot{o}$6976 and PD98059) promoted apoptosis. Conclusion: Resveratrol has significant anti-proliferative effects on the colon cancer cell line HT-29. The PKC-ERK1/2 signaling pathway can partially mediate resveratrol-induced apoptosis of HT-29 cells.