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PI3K-Akt/mTOR通路调控P-β-catenin介导溃疡性结肠炎相关癌变及健脾清热活血方防治研究

A review on the mechanism of Jian Pi Qing Re Huo Xue decoction preventing the onset of UCAC by mediating PI3K - Akt /mTOR signal pathway

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【作者】 张涛黄会云曹火留陈远能王小平潘怀耿张志明

【Author】 ZHANG Tao1,HUANG Hui-yun1,CAO Huo-liu1,CHEN Yuan-neng1,WANG Xiao-ping2,PAN Huai-geng3,ZHANG Zhi-ming4(1.The Rui Kang Hospital Affiliated Guangxi University of TCM,Nanning 530011,China;2.The Jiangxi College of TCM,Fuzhou 3447003,China,;3.Guangzhou University of TCM,Guangzhou 510000,China;4.Shunde Professional Technology college,Shunde 528300,China)

【机构】 广西中医药大学附属瑞康医院江西中医药高等专科学校广州中医药大学顺德职业技术学院

【摘要】 溃疡性结肠炎相关性结肠癌(ulcerative colitis associated cancer,UCAC)是溃疡性结肠炎(ulcerative colitis,UC或溃结)患者重要死亡原因,其癌变具体机制尚未明了。β-catenin磷酸化及其核内异常转位被认为是UCAC关键事件之一,经典Wnt通路以及炎症状态下PI3K-Akt/mTOR通路过度活化、突变均可导致β-catenin不被泛素化降解,反而大量磷酸化、核内异常转位,下游靶基因过度转录,肠上皮细胞凋亡、增殖、甚至异性增生、癌变。文章就近年来关于PI3K-Akt/mTOR通路调控P-β-catenin介导UCAC,以及我们研究健脾清热活血方药干预UCAC的相关研究进行述评。

【Abstract】 The most important cause of death in ulcerative colitis is ulcerative colitis associated cancer.However,the mechanism of carcinogenesis is unknown.There is a sign that phosphorylation of β-catenin and nuclear abnormal translocation involve in multi-signal pathway.Except the canonical Wnt / β-catenin pathway,we put forward a hypothesis that excessive activation of PI3K / Akt-mTOR after EGF combined with EGFR plays an important role in the onset of UCAC under inflammation.That signal pathway we have mentioned above which cooperative with Wnt signal pathway induce excessive phosphorylation of β-catenin which may lead to downstream target gene excessive transcription.This paper is review on the mechanism of Jian Pi Qing Re Huo Xue decoction preventing the onset of UCAC by mediating PI3K-Akt / mTOR signal pathway.

【基金】 国家自然科学基金青年基金(No.81001507);国家自然科学基金面上项目(No.81260536);广西卫生厅重点项目(No.2011041)
  • 【文献出处】 时珍国医国药 ,Lishizhen Medicine and Materia Medica Research , 编辑部邮箱 ,2013年08期
  • 【分类号】R273;R259
  • 【被引频次】16
  • 【下载频次】708
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