临床肿瘤学杂志

• 综述与讲座 • 上一篇    下一篇

HIF-1α在光动力治疗肿瘤中的研究进展

蒋彩玲,白玉贤,李燕京,谢 蕊

  

  1. 150081 哈尔滨 哈尔滨医科大学附属肿瘤医院消化内科
  • 收稿日期:2014-05-21 修回日期:2014-09-23 出版日期:2014-12-31 发布日期:2014-12-31
  • 通讯作者: 白玉贤

Progression of hypoxiainducible factor-1 alpha in photodynamic therapy of tumor

JIANG Cailing, BAI Yuxian, LI Yanjing, XIE Rui.

  

  1. Department of Gastroenterology, Cancer Hospital Affiliated to Harbin Medical University, Harbin 150081, China
  • Received:2014-05-21 Revised:2014-09-23 Online:2014-12-31 Published:2014-12-31
  • Contact: BAI Yuxian

摘要: 全球恶性肿瘤的发病率和死亡率在不断升高,危害愈来愈大,引起全社会的广泛重视。现在多数治疗如手术、放疗、化疗由于有一定副作用都会给患者机体带来相当负担,所以要充分衡量增加一种治疗可能给患者带来的得与失。光动力治疗作为一种新型的肿瘤治疗技术,以其独特的靶向性、无耐药性等,引起越来越多学者的关注。研究表明,光动力杀伤肿瘤细胞是由多种机制介导的,除了已知的坏死和凋亡机制外,光动力诱导产生的炎性反应也能够间接有利于肿瘤细胞的清除。缺氧诱导因子1α(HIF-1α)是具有转录活性的核蛋白,具有相当广泛的靶基因谱(如缺氧适应、炎症发展及肿瘤生长),其中所包括的血管内皮生长因子是最重要的促进血管化的基因之一。本文就近年HIF-1α在光动力治疗肿瘤细胞中的研究进展作一综述。

Abstract: Malignant tumors have become the leading cause of human death. Conventional anticancer treatment modalities, such as surgery, radiation and chemotherapy, are often deleterious to the patient due to the numerous associated side effects. Photodynamic therapy(PDT) as a new approach available to cancer therapy, with its unique targeting and nondrug resistance, caused more and more attention of scholars. Previous studies have shown that PDT destructed tumor by a variety of mechanisms. In addition to the known mechanism of necrosis and apoptosis, inflammatory reaction after PDT can also indirectly help the removal of tumor cells. Hypoxiainducible factor-1alpha(HIF-1α) is a nucleoprotein with transcriptional activity, possessing a wide spectrum of target genes(such as hypoxia adaptation, inflammation development and tumor growth), which include vascular endothelial growth factor(VEGF), one of the most important genes in promoting vascularization. In this review, we discuss the role of HIF-1α in the PDT of tumor cells.

No related articles found!
Viewed
Full text


Abstract

Cited

  Shared   
  Discussed   
No Suggested Reading articles found!