Cyclooxygenase-2 Induction by Amino Acid Deprivation Requires p38 Mitogen-Activated Protein Kinase in Human Glioma Cells

被引：5
|
作者：
Li, Zhiwen [1 ,2 ,3 ]
Chang, Chi-Ming [1 ,2 ]
Wang, Lanfang [1 ,2 ]
Zhang, Ping [4 ]
Shu, Hui-Kuo G. [1 ,2 ]
机构：
[1] Emory Univ, Dept Radiat Oncol, Atlanta, GA 30322 USA
[2] Emory Univ, Winship Canc Inst, Atlanta, GA 30322 USA
[3] Jilin Univ, Hosp 1, Dept Anesthesiol, Changchun, Peoples R China
[4] Jilin Univ, Hosp 1, Dept Hepatobiliary & Pancreat Surg, Changchun 130021, Jilin, Peoples R China
来源：
CANCER INVESTIGATION | 2017年 / 35卷 / 04期
关键词：
Glioblastomas; amino acid deprivation; COX-2; p38-MAPK; VEGF; GROWTH-FACTOR EXPRESSION; ADJUVANT TEMOZOLOMIDE; COX-2; INHIBITOR; GLIOBLASTOMA; CANCER; CELECOXIB; AUTOPHAGY; HYPOXIA; RADIOTHERAPY; ANGIOGENESIS;
D O I：
10.1080/07357907.2017.1292517
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
Glioblastomas (GBMs) are malignant brain tumors that can outstrip nutrient supplies due to rapid growth. Cyclooxygenase-2 (COX-2) has been linked to GBMs and may contribute to their aggressive phenotypes. Amino acid starvation results in COX-2 mRNA and protein induction in multiple human glioma cell lines in a process requiring p38 mitogen-activated protein kinase (p38-MAPK) and the Sp1 transcription factor. Increased vascular endothelial growth factor expression results from starvation-dependent COX-2 induction. These data suggest that COX-2 induction with amino acid deprivation may be a part of the adaptation of glioma cells to these conditions, and potentially alter cellular response to anti-neoplastic therapy.
引用
收藏
页码：237 / 247
页数：11
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