临床肿瘤学杂志

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PGE2通过EP1受体促进肝癌细胞生长和侵袭的研究进展

宋梦颖,杨沁怡,张智弘   

  1. 210029 南京 南京医科大学第一附属医院病理科
  • 收稿日期:2016-08-10 修回日期:2016-10-08 出版日期:2017-01-30 发布日期:2017-01-30
  • 通讯作者: 张智弘

Prostaglandin E2 promotes hepatic cancer cell growth and invasion via receptor EP1

SONG Mengying, YANG Qinyi, ZHANG Zhihong.
  

  1. Department of Pathology, the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China
  • Received:2016-08-10 Revised:2016-10-08 Online:2017-01-30 Published:2017-01-30
  • Contact: ZHANG Zhihong

摘要: 前列腺素E2(PGE2)是一种参与肝癌细胞生长与侵袭的重要细胞因子。PGE2通过与细胞膜表面的EP受体结合来发挥其调控肿瘤发生、发展的作用。在肝癌中,PGE2通过前列腺素E受体1(EP1)受体调节EGFR/PI3K/Akt、Src/EGFR/p44/42 MAPK/mTOR等信号通路影响Survivin、YB-1等关键物质,促进肝癌细胞生长和侵袭。现就近年来PGE2通过EP1受体促进肝癌细胞生长和侵袭作用机制的研究进行综述。

Abstract: Prostaglandin E2 (PGE2) has been proposed as an important cellular factor associated with hepatic cancer cell growth and invasion. PGE2 regulates tumor development and progression by combining with E prostanoid receptors (EP receptors) on the surface of the cell membrane. PGE2 exerts its effects by upregulating the expression of key molecules including survivin and YB-1, in hepatic cancer cells. PGE2 regulates survivin expression through EP1/EGFR/PI3K/Akt signaling pathway, and YB-1 expression through EP1/Src/EGFR/p44/42 MAPK/mTOR signaling pathway. In this review, we discuss the mechanism of prostaglandin E2 promoting hepatic cancer cell growth and invasion via receptor EP1, which may represent a new therapeutic strategy for the prevention and treatment of hepatic cancer.

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