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中华胸部外科电子杂志 ›› 2016, Vol. 03 ›› Issue (03) : 177 -181. doi: 10.3877/cma.j.issn.2095-8773.2016.03.10

所属专题: 文献

综述

PEBP4蛋白的表达及与肺鳞状细胞癌分化转移的关系
虞桂平1,()   
  1. 1. 214400 东南大学医学院附属江阴医院胸心外科
  • 收稿日期:2016-03-10 出版日期:2016-08-28
  • 通信作者: 虞桂平
  • 基金资助:
    江苏省第四期"333工程"培养资金资助(BRA2014043)

Expression of PEBP4 protein and its relationship with differentiation and metastasis of squamous cell carcinoma of lung

Guiping Yu1,()   

  1. 1. Department of Thoracic and Cardiac Surgery, Jiangyin Hospital, Medical College of Southeast University, Jiangyin 214400, China
  • Received:2016-03-10 Published:2016-08-28
  • Corresponding author: Guiping Yu
  • About author:
    Corresponding author:Yu Guiping,Email:
引用本文:

虞桂平. PEBP4蛋白的表达及与肺鳞状细胞癌分化转移的关系[J/OL]. 中华胸部外科电子杂志, 2016, 03(03): 177-181.

Guiping Yu. Expression of PEBP4 protein and its relationship with differentiation and metastasis of squamous cell carcinoma of lung[J/OL]. Chinese Journal of Thoracic Surgery(Electronic Edition), 2016, 03(03): 177-181.

肺癌是一种严重威胁人类健康的疾病,尤其是肺鳞状细胞癌。因此,必须寻找更加精确、有效的分子标志物,为肺癌的早期发现、预后判断以及靶向治疗等提供科学依据。PEBP4属于磷脂酰乙醇胺结合蛋白(PEBP)家族的成员,不仅参与MAPK信号通路的抑制作用,还参与JNK通路的抑制,促进AKT的激活。最近研究资料还显示,PEBP4蛋白的过表达与多种肿瘤的发生、发展以及侵润转移相关。该文对PEBP4表达与肺鳞状细胞癌分化转移的关系进行了综述。

Lung cancer, especiallysquamous cell carcinoma of lung, is a diseasewhich posesserious threat to human beings. Therefore, more accurate and effective molecular markersshould befoundin order to provide a scientific basis forthe early detection, prognosisprediction and targeted therapyof lung cancer. Phosphatidylethanolamine-binding protein 4 (PEBP4) belongs to the phosphatidylethanolamine binding protein family members, whichnot onlyinhibitsthe MAPK signaling pathway, but also participatesin the inhibition of JNK pathway andpromotion of AKTactivation. It has been recently reported thattheoverexpression of PEBP4 protein is relatedtothe development and metastasis of a variety of tumors. This review discusses the relationship between the expression of PEBP4 and differentiation and metastasis of squamous cell carcinoma of lung.

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