Programmed death-ligand 1 (PD-L1) may play a role in malignant glioma infiltration

被引：4
作者：
Zhang, Lei [1 ]
Zhang, Zhiqing [2 ]
Liu, Yunhui [1 ]
Xue, Yixue [3 ]
Parney, Ian [4 ]
机构：
[1] China Med Univ, Shengjing Hosp, Dept Neurosurg, Shenyang, Liaoning, Peoples R China
[2] Univ Wisconsin, Madison, WI 53706 USA
[3] China Med Univ, Dept Neurobiol, Shenyang, Liaoning, Peoples R China
[4] Mayo Clin, Dept Neurosurg, Rochester, MN USA
来源：
MEDICAL HYPOTHESES | 2015年 / 85卷 / 02期
关键词：
B7 FAMILY MOLECULES; TUMOR-CELLS; B7-H1; EXPRESSION; INVASION; CANCER; PREGNANCY; MECHANISM; GROWTH; MODEL;
D O I：
10.1016/j.mehy.2015.04.009
中图分类号：
R-3 [医学研究方法]; R3 [基础医学];
学科分类号：
1001 ;
摘要：
Infiltration is the main cause of death of malignant glioma patients. However, the mechanisms of the infiltration in the development of brain cancer (glioblastoma multiforme) are not completely understood. Here, we hypothesized that, in the development of human brain cancer, infiltration is primarily due to differentiated cancer cells and that the cell surface molecule programmed death-ligand 1 (PD-L1) may play an important role in brain tumor infiltration. PD-L1 is highly expressed in differentiated glioma cells in comparison to undifferentiated ones. As PD-L1 has both pro-survival and immunoinhibitory functions in tumor cells, the potential role of PD-L1 in tumor propagation suggest a new therapeutic target for preventing glioma infiltration and recurrence. (C) 2015 Elsevier Ltd. All rights reserved.
引用
收藏
页码：127 / 129
页数：3
相关论文
共 20 条
[1]   B7-H1 Overexpression Regulates Epithelial-Mesenchymal Transition and Accelerates Carcinogenesis in Skin [J].
Cao, Yujia ;
Zhang, Lu ;
Kamimura, Yosuke ;
Ritprajak, Patcharee ;
Hashiguchi, Masaaki ;
Hirose, Sachiko ;
Azuma, Miyuki .
CANCER RESEARCH, 2011, 71 (04) :1235-1243
[2]   Tumor cells disseminate early, but immunosurveillance limits metastatic outgrowth, in a mouse model of melanoma [J].
Eyles, Jo ;
Puaux, Anne-Laure ;
Wang, Xiaojie ;
Toh, Benjamin ;
Prakash, Celine ;
Hong, Michelle ;
Tan, Tze Guan ;
Zheng, Lin ;
Ong, Lai Chun ;
Jin, Yi ;
Kato, Masashi ;
Prevost-Blondel, Armelle ;
Chow, Pierce ;
Yang, Henry ;
Abastado, Jean-Pierre .
JOURNAL OF CLINICAL INVESTIGATION, 2010, 120 (06) :2030-2039
[3]  
Fisher S J, 1993, Semin Cell Biol, V4, P183, DOI 10.1006/scel.1993.1022
[4]   Malignant astrocytic glioma: genetics, biology, and paths to treatment [J].
Furnari, Frank B. ;
Fenton, Tim ;
Bachoo, Robert M. ;
Mukasa, Akitake ;
Stommel, Jayne M. ;
Stegh, Alexander ;
Hahn, William C. ;
Ligon, Keith L. ;
Louis, David N. ;
Brennan, Cameron ;
Chin, Lynda ;
DePinho, Ronald A. ;
Cavenee, Webster K. .
GENES & DEVELOPMENT, 2007, 21 (21) :2683-2710
[5]   Expression of B7-H1 in breast cancer patients is strongly associated with high proliferative Ki-67-expressing tumor cells [J].
Ghebeh, Hazem ;
Tulbah, Asma ;
Mohammed, Shamayel ;
Eikum, Naser ;
Bin Amer, Suad M. ;
Al-Tweigeri, Taber ;
Dermime, Said .
INTERNATIONAL JOURNAL OF CANCER, 2007, 121 (04) :751-758
[6]  
HIROSHI F, 2005, REPROD MED BIOL, V4, P189
[7]  
Holtan SG, 2009, MAYO CLIN PROC, V84, P985, DOI 10.1016/S0025-6196(11)60669-1
[8]   Blockade of B7-H1 or B7-DC induces an anti-tumor effect in a mouse pancreatic cancer model [J].
Okudaira, Keisuke ;
Hokari, Ryota ;
Tsuzuki, Yoshikazu ;
Okada, Yoshikiyo ;
Komoto, Shunsuke ;
Watanabe, Chikako ;
Kurihara, Chie ;
Kawaguchi, Atsushi ;
Nagao, Shigeaki ;
Azuma, Miyuki ;
Yagita, Hideo ;
Miura, Soichiro .
INTERNATIONAL JOURNAL OF ONCOLOGY, 2009, 35 (04) :741-749
[9]   Loss of tumor suppressor PTEN function increases B7-H1 expression and immunoresistance in glioma [J].
Parsa, Andrew T. ;
Waldron, James S. ;
Panner, Amith ;
Crane, Courtney A. ;
Parney, Ian F. ;
Barry, Jeffrey J. ;
Cachola, Kristine E. ;
Murray, Joseph C. ;
Tihan, Tarik ;
Jensen, Michael C. ;
Mischel, Paul S. ;
Stokoe, David ;
Pieper, Russell O. .
NATURE MEDICINE, 2007, 13 (01) :84-88
[10]   B7 Family Molecules as Regulators of the Maternal Immune System in Pregnancy [J].
Petroff, Margaret G. ;
Perchellet, Antoine .
AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, 2010, 63 (06) :506-519
12