Expression of Toll-Like Receptors on Breast Tumors: Taking a Toll on Tumor Microenvironment

被引:41
作者
Bhattacharya, Debika [1 ,2 ]
Yusuf, Nabiha [1 ,2 ,3 ,4 ]
机构
[1] Univ Alabama Birmingham, Dept Dermatol, 1670 Univ Blvd,VH 566A,POB 202, Birmingham, AL 35294 USA
[2] Univ Alabama Birmingham, Skin Dis Res Ctr, Birmingham, AL 35294 USA
[3] Univ Alabama Birmingham, Vet Affairs Med Ctr, Birmingham, AL 35294 USA
[4] Univ Alabama Birmingham, Comprehens Canc Ctr, Birmingham, AL 35294 USA
关键词
D O I
10.1155/2012/716564
中图分类号
R73 [肿瘤学];
学科分类号
100214 [肿瘤学];
摘要
Breast cancer remains a major cause of death in women in the developed world. As Toll-like receptors ( TLRs) are widely expressed on tumor cells and play important roles in the initiation and progression of cancer, they may thus serve as important targets and have an effective perspective on breast cancer treatment. Expression of TLRs on breast cancer cells and mononuclear inflammatory cells can promote inflammation and cell survival in the tumor microenvironment. Inflammation and cancer are related. It is well known that persistent inflammatory conditions can induce cancer formation, due to production of cytokines and chemokines, which play a crucial role in promoting angiogenesis, metastasis, and subversion of adaptive immunity. TLR signaling in tumor cells can mediate tumor cell immune escape and tumor progression, and it is regarded as one of the mechanisms for chronic inflammation in tumorigenesis and progression. This paper delineates the expression of various TLRs in promotion of inflammation and development of mammary tumors. Understanding the mechanisms through which TLRs on breast cancer cells and inflammatory cells regulate growth, survival, and metastatic progression can make them potential targets for breast cancer therapy.
引用
收藏
页数:6
相关论文
共 49 条
[1]
Pathogen recognition and innate immunity [J].
Akira, S ;
Uematsu, S ;
Takeuchi, O .
CELL, 2006, 124 (04) :783-801
[2]
Recognition of double-stranded RNA and activation of NF-κB by Toll-like receptor 3 [J].
Alexopoulou, L ;
Holt, AC ;
Medzhitov, R ;
Flavell, RA .
NATURE, 2001, 413 (6857) :732-738
[3]
Cell activation and apoptosis by bacterial lipoproteins through toll-like receptor-2 [J].
Aliprantis, AO ;
Yang, RB ;
Mark, MR ;
Suggett, S ;
Devaux, B ;
Radolf, JD ;
Klimpel, GR ;
Godowski, P ;
Zychlinsky, A .
SCIENCE, 1999, 285 (5428) :736-739
[4]
The Yin-Yang of tumor-associated macrophages in neoplastic progression and immune surveillance [J].
Allavena, Paola ;
Sica, Antonio ;
Garlanda, Cecilia ;
Mantovani, Alberto .
IMMUNOLOGICAL REVIEWS, 2008, 222 :155-161
[5]
American Cancer Society, 2011, BREAST CANC FACTS FI
[6]
Neo-ligands for innate immune receptors and the etiology of sterile inflammatory disease [J].
Beutler, Bruce .
IMMUNOLOGICAL REVIEWS, 2007, 220 :113-128
[7]
DAMPs, PAMPs and alarmins: all we need to know about danger [J].
Bianchi, Marco E. .
JOURNAL OF LEUKOCYTE BIOLOGY, 2007, 81 (01) :1-5
[8]
Activation of Toll-like Receptor 5 on Breast Cancer Cells by Flagellin Suppresses Cell Proliferation and Tumor Growth [J].
Cai, Zhenyu ;
Sanchez, Amir ;
Shi, Zhongcheng ;
Zhang, Tingting ;
Liu, Mingyao ;
Zhang, Dekai .
CANCER RESEARCH, 2011, 71 (07) :2466-2475
[9]
Inflammation and cancer [J].
Coussens, LM ;
Werb, Z .
NATURE, 2002, 420 (6917) :860-867
[10]
TLRs, NLRs and RLRs: a trinity of pathogen sensors that co-operate in innate immunity [J].
Creagh, Emma M. ;
O'Neill, Luke A. J. .
TRENDS IN IMMUNOLOGY, 2006, 27 (08) :352-357