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编号:11319634
COX-2抑制剂NS398调控PPARs信号转导通路抑制结肠癌细胞增殖的分子机制
http://www.100md.com 余力伟, 马向涛
结直肠肿瘤;信号转导;过氧化物酶体增殖因子激活受体;COX-2余力伟,马向涛.COX-2抑制剂NS398调控PPARs信号转导通路抑制结肠癌细胞增殖的分子机制. 世界华人消化杂志2006;
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     余力伟, 马向涛, 北京市海淀医院外科 北京市 100080

    余力伟,
副主任医师, 主要从事消化系统肿瘤研究.

    通讯作者:
马向涛, 100080, 北京市海淀区中关村大街29号, 北京市海淀医院外科. xiangtao_ma@pku.org.cn

    电话:
010-62583013 传真: 010-62653601

    收稿日期:
2006-07-30 接受日期: 2006-08-22

    Molecular mechanism of cyclooxygenase-2 inhibitor in regulating proliferation of colon cancer cells through modulating PPAR signal transduction pathway

    Li-Wei Yu, Xiang-Tao Ma

    Li-Wei Yu, Xiang-Tao Ma, Department of Surgery, Beijing Haidian Hospital, Beijing 10080, China

    Correspondence to:
Dr. Xiang-Tao Ma, Department of Surgery, Beijing Haidian Hospital, 29 Zhongguancun Avenue, Beijing 100080, China. xiangtao_ma@pku.org.cn

    Received:
2006-07-30 Accepted: 2006-08-22

    Abstract

    AIM:
To investigate the role of selective cyclooxygenase-2 (COX-2) inhibitor NS398 on the proliferation and apoptosis of colorectal cancer cells, and reveal the COX-2-independent mechanism.

    METHODS: Reverse transcription-polymerase chain reaction (RT-PCR) was performed on human colon cancer cell line SW480 to examine COX-2 mRNA expression. Then, NS-398 (a selective COX-2 inhibitor) was added into culture media, and MTT assay was used to examine the proliferation of the cells; Western blot analysis was performed to detect the expression of peroxisome proliferators-activated receptor (PPAR); Flow cytometry was applied to analyze the cell cycle and apoptosis.

    RESULTS: The expression of COX-2 mRNA was not detected in colon cancer SW480 cells. NS-398 inhibited the cell proliferation and induced apoptosis in colon cancer cell lines. Seventy-two hours after the treatment of NS398 (75 mmol/L), the proliferative level of SW480 cells was decreased; the rate of the cells at G1 stage was increased from 31.2% to 40.6%, while the rate of those at S stage was decreased from 52.8% to 41.2%. The expression of PPARa, PPARd, PPARg, cyclin D1 and Bcl-xl were decreased along with the prolonging of NS398 treated time ......

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