STATs in cancer inflammation and immunity: a leading role for STAT3

被引:3943
作者
Yu, Hua [1 ]
Pardoll, Drew [2 ]
Jove, Richard [1 ]
机构
[1] City Hope Comprehens Canc Ctr, Beckman Res Inst, Duarte, CA 91010 USA
[2] Sidney Kimmel Comprehens Canc Ctr, Johns Hopkins Sch Med, Baltimore, MD 20892 USA
关键词
NF-KAPPA-B; REGULATORY T-CELLS; EPIDERMAL-GROWTH-FACTOR; HYPER-IGE SYNDROME; COLITIS-ASSOCIATED CANCER; POTENT ANTITUMOR-ACTIVITY; DNA-BINDING ACTIVITY; SIGNAL TRANSDUCER; TRANSCRIPTION; GENE-EXPRESSION;
D O I
10.1038/nrc2734
中图分类号
R73 [肿瘤学];
学科分类号
100214 [肿瘤学];
摘要
Commensurate with their roles in regulating cytokine-dependent inflammation and immunity, signal transducer and activator of transcription ( STAT) proteins are central in determining whether immune responses in the tumour microenvironment promote or inhibit cancer. Persistently activated STAT3 and, to some extent, STAT5 increase tumour cell proliferation, survival and invasion while suppressing anti-tumour immunity. The persistent activation of STAT3 also mediates tumour-promoting inflammation. STAT3 has this dual role in tumour inflammation and immunity by promoting pro-oncogenic inflammatory pathways, including nuclear factor-kappa B (NF-kappa B) and interleukin-6 (IL-6)-GP130-Janus kinase (JAK) pathways, and by opposing STAT1- and NF-kappa B-mediated T helper 1 anti-tumour immune responses. Consequently, STAT3 is a promising target to redirect inflammation for cancer therapy.
引用
收藏
页码:798 / 809
页数:12
相关论文
共 157 条
[1]
MOLECULAR-CLONING OF APRF, A NOVEL IFN-STIMULATED GENE FACTOR-3 P91-RELATED TRANSCRIPTION FACTOR INVOLVED IN THE GP130-MEDIATED SIGNALING PATHWAY [J].
AKIRA, S ;
NISHIO, Y ;
INOUE, M ;
WANG, XJ ;
WEI, S ;
MATSUSAKA, T ;
YOSHIDA, K ;
SUDO, T ;
NARUTO, M ;
KISHIMOTO, T .
CELL, 1994, 77 (01) :63-71
[2]
Defects along the TH17 differentiation pathway underlie genetically distinct forms of the hyper IgE syndrome [J].
Al Khatib, Shadi ;
Keles, Sevgi ;
Garcia-Lioret, Maria ;
Koc-Aydiner, Elif Kara ;
Reisli, Ismail ;
Artac, Hasibe ;
Camcioglu, Yildiz ;
Cokugras, Haluk ;
Somer, Ayper ;
Kutukculer, Necil ;
Yilmaz, Mustafa ;
Ikinciogullari, Aydan ;
Yegin, Olcay ;
Yuksek, Mutlu ;
Genel, Ferah ;
Kucukosmanoglu, Ercan ;
Baki, Ali ;
Bahceciler, Nerin N. ;
Rambhatla, Anupama ;
Nickerson, Derek W. ;
McGhee, Sean ;
Barlan, Isil B. ;
Chatila, Talal .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 2009, 124 (02) :342-348
[3]
Interleukin-6 in the Bone Marrow Microenvironment Promotes the Growth and Survival of Neuroblastoma Cells [J].
Ara, Tasnim ;
Song, Liping ;
Shimada, Hiroyuki ;
Keshelava, Nino ;
Russell, Heidi V. ;
Metelitsa, Leonid S. ;
Groshen, Susan G. ;
Seeger, Robert C. ;
DeClerck, Yves A. .
CANCER RESEARCH, 2009, 69 (01) :329-337
[4]
Receptor-mediated tobacco toxicity:: cooperation of the Ras/Raf-1/MEK1/ERK and JAK-2/STAT-3 pathways downstream of α7 nicotinic receptor in oral keratinocytes [J].
Arredondo, Juan ;
Chernyavsky, Alexander I. ;
Jolkovsky, David L. ;
Pinkerton, Kent E. ;
Grando, Sergei A. .
FASEB JOURNAL, 2006, 20 (12) :2093-2101
[5]
Protein kinase Cε, which sensitizes skin to sun's UV radiation-induced cutaneous damage and development of squamous cell carcinomas, associates with Stat3 [J].
Aziz, Moammir H. ;
Manoharan, Herbert T. ;
Verma, Ajit K. .
CANCER RESEARCH, 2007, 67 (03) :1385-1394
[6]
VEGF differentially activates STAT3 in microvascular endothelial cells [J].
Bartoli, M ;
Platt, DH ;
Lemtalsi, T ;
Gu, XL ;
Brooks, SE ;
Marrero, MB ;
Caldwell, RB .
FASEB JOURNAL, 2003, 17 (09) :1562-+
[7]
Barton BE, 2004, MOL CANCER THER, V3, P11
[8]
Nuclear factor-κB and inhibitor of κB kinase pathways in oncogenic initiation and progression [J].
Basseres, D. S. ;
Baldwin, A. S. .
ONCOGENE, 2006, 25 (51) :6817-6830
[9]
Battle T. E., 2002, Current Molecular Medicine (Hilversum), V2, P381, DOI 10.2174/1566524023362456
[10]
OPINION Is NF-κB a good target for cancer therapy? Hopes and pitfalls [J].
Baud, Veronique ;
Karin, Michael .
NATURE REVIEWS DRUG DISCOVERY, 2009, 8 (01) :33-40