Tumour endothelial cells acquire drug resistance in a tumour microenvironment

被引：56

作者：

Hida, Kyoko ^{[1
]}

Akiyama, Kosuke ^{[1
]}

Ohga, Noritaka ^{[1
]}

Maishi, Nako ^{[1
]}

Hida, Yasuhiro ^{[2
]}

机构：

[1] Hokkaido Univ, Dept Vasc Biol, Grad Sch Dent Med, Sapporo, Hokkaido 0608586, Japan

[2] Hokkaido Univ, Dept Cardiovasc & Thorac Surg, Grad Sch Med, Sapporo, Hokkaido 0608586, Japan

来源：

JOURNAL OF BIOCHEMISTRY | 2013年 / 153卷 / 03期

关键词：

angiogenesis; anti-angiogenic therapy; drug resistance; endothelial cells; tumours; PHASE-II TRIAL; P-GLYCOPROTEIN; METRONOMIC CHEMOTHERAPY; ANTIANGIOGENIC THERAPY; MULTIDRUG-RESISTANCE; CANCER; ANGIOGENESIS; SURVIVAL; KINASE; GROWTH;

D O I：

10.1093/jb/mvs152

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Tumour growth is dependent on angiogenesis, and tumour blood vessels are recognized as an important target for cancer therapy. Tumour endothelial cells (TECs) are the main targets of anti-angiogenic therapy. Unlike the traditionally held view, some TECs may be genetically abnormal and might acquire drug resistance. Therefore, we investigated the drug resistance of TECs and the mechanism by which it is acquired. TECs show resistance to paclitaxel through greater mRNA expression of multidrug resistance 1, which encodes P-glycoprotein, as compared with normal endothelial cells. We found that high levels of vascular endothelial growth factor in tumour-conditioned medium may be responsible for upregulated P-glycoprotein expression. This is a novel mechanism for the acquisition of drug resistance by TECs in a tumour microenvironment. This review focuses on the possibility that TECs can acquire drug resistance.

引用

页码：243 / 249

页数：7

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