HMGB1 in Cancer: Good, Bad, or Both?

被引：422

作者：

Kang, Rui ^{[1
]}

Zhang, Qiuhong ^{[1
]}

Zeh, Herbert J., III ^{[1
]}

Lotze, Michael T. ^{[1
,2
,3
]}

Tang, Daolin ^{[1
]}

机构：

[1] Univ Pittsburgh, Inst Canc, Dept Surg, Hillman Canc Ctr, Pittsburgh, PA 15232 USA

[2] Univ Pittsburgh, Inst Canc, Dept Immunol, Hillman Canc Ctr, Pittsburgh, PA 15232 USA

[3] Univ Pittsburgh, Inst Canc, Dept Bioengn, Hillman Canc Ctr, Pittsburgh, PA 15232 USA

来源：

CLINICAL CANCER RESEARCH | 2013年 / 19卷 / 15期

关键词：

GLYCATION END-PRODUCTS; GROUP BOX 1; CHROMATIN PROTEIN HMGB1; TUMOR PROGRESSION; CELL RECRUITMENT; IMMUNE-RESPONSES; AUTOPHAGY; RECEPTOR; RAGE; EXPRESSION;

D O I：

10.1158/1078-0432.CCR-13-0495

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Forty years ago, high mobility group box 1 (HMGB1) was discovered in calf thymus and named according to its electrophoretic mobility in polyacrylamide gels. Now, we know that HMGB1 performs dual functions. Inside the cell, HMGB1 is a highly conserved chromosomal protein acting as a DNA chaperone. Outside of the cell, HMGB1 is a prototypical damage-associated molecular pattern, acting with cytokines, chemokines, and growth factors. During tumor development and in cancer therapy, HMGB1 has been reported to play paradoxical roles in promoting both cell survival and death by regulating multiple signaling pathways, including inflammation, immunity, genome stability, proliferation, metastasis, metabolism, apoptosis, and autophagy. Here, we review the current knowledge of both HMGB1's oncogenic and tumor-suppressive roles and the potential strategies that target HMGB1 for the prevention and treatment of cancer. (C) 2013 AACR.

引用

页码：4046 / 4057

页数：12

共 75 条

[1] HMGB1 Is a Therapeutic Target for Sterile Inflammation and Infection [J].

Andersson, Ulf ;

Tracey, Kevin J. .

ANNUAL REVIEW OF IMMUNOLOGY, VOL 29, 2011, 29 :139-162

[2] Toll-like receptor 4-dependent contribution of the immune system to anticancer chemotherapy and radiotherapy [J].

Apetoh, Lionel ;

Ghiringhelli, Francois ;

Tesniere, Antoine ;

Obeid, Michel ;

Ortiz, Carla ;

Criollo, Alfredo ;

Mignot, Gregoire ;

Maiuri, M. Chiara ;

Ullrich, Evelyn ;

Saulnier, Patrick ;

Yang, Huan ;

Amigorena, Sebastian ;

Ryffel, Bernard ;

Barrat, Franck J. ;

Saftig, Paul ;

Levi, Francis ;

Lidereau, Rosette ;

Nogues, Catherine ;

Mira, Jean-Paul ;

Chompret, Agnes ;

Joulin, Virginie ;

Clavel-Chapelon, Francoise ;

Bourhis, Jean ;

Andre, Fabrice ;

Delaloge, Suzette ;

Tursz, Thomas ;

Kroemer, Guido ;

Zitvogel, Laurence .

NATURE MEDICINE, 2007, 13 (09) :1050-1059

[3] The extracellular release of HMGB1 during apoptotic cell death [J].

Bell, Charles W. ;

Jiang, Weiwen ;

Reich, Charles F., III ;

Pisetsky, David S. .

AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, 2006, 291 (06) :C1318-C1325

[4] Monocytic cells hyperacetylate chromatin protein HMGB1 to redirect it towards secretion [J].

Bonaldi, T ;

Talamo, F ;

Scaffidi, P ;

Ferrera, D ;

Porto, A ;

Bachi, A ;

Rubartelli, A ;

Agresti, A ;

Bianchi, ME .

EMBO JOURNAL, 2003, 22 (20) :5551-5560

[5] HMGB1: a two-headed signal regulating tumor progression and immunity [J].

Campana, Lara ;

Bosurgi, Lidia ;

Rovere-Querini, Patrizia .

CURRENT OPINION IN IMMUNOLOGY, 2008, 20 (05) :518-523

[6] Substantial Histone Reduction Modulates Genomewide Nucleosomal Occupancy and Global Transcriptional Output [J].

Celona, Barbara ;

Weiner, Assaf ;

Di Felice, Francesca ;

Mancuso, Francesco M. ;

Cesarini, Elisa ;

Rossi, Riccardo L. ;

Gregory, Lorna ;

Baban, Dilair ;

Rossetti, Grazisa ;

Grianti, Paolo ;

Pagani, Massimiliano ;

Bonaldi, Tiziana ;

Ragoussis, Jiannis ;

Friedman, Nir ;

Camilloni, Giorgio ;

Bianchi, Marco E. ;

Agresti, Alessandra .

PLOS BIOLOGY, 2011, 9 (06)

[7] CD24 and Siglec-10 Selectively Repress Tissue Damage-Induced Immune Responses [J].

Chen, Guo-Yun ;

Tang, Jie ;

Zheng, Pan ;

Liu, Yang .

SCIENCE, 2009, 323 (5922) :1722-1725

[8] Tumor-infiltrating DCs suppress nucleic acid-mediated innate immune responses through interactions between the receptor TIM-3 and the alarmin HMGB1 [J].

Chiba, Shigeki ;

Baghdadi, Muhammad ;

Akiba, Hisaya ;

Yoshiyama, Hironori ;

Kinoshita, Ichiro ;

Dosaka-Akita, Hirotoshi ;

Fujioka, Yoichiro ;

Ohba, Yusuke ;

Gorman, Jacob V. ;

Colgan, John D. ;

Hirashima, Mitsuomi ;

Uede, Toshimitsu ;

Takaoka, Akinori ;

Yagita, Hideo ;

Jinushi, Masahisa .

NATURE IMMUNOLOGY, 2012, 13 (09) :832-842

[9] Chemotherapy response of spontaneous mammary tumors is independent of the adaptive immune system [J].

Ciampricotti, Metamia ;

Hau, Cheei-Sing ;

Doornebal, Chris W. ;

Jonkers, Jos ;

de Visser, Karin E. .

NATURE MEDICINE, 2012, 18 (03) :344-346

[10] HMGB1 Mediates Endogenous TLR2 Activation and Brain Tumor Regression [J].

Curtin, James F. ;

Liu, Naiyou ;

Candolfi, Marianela ;

Xiong, Weidong ;

Assi, Hikmat ;

Yagiz, Kader ;

Edwards, Matthew R. ;

Michelsen, Kathrin S. ;

Kroeger, Kurt M. ;

Liu, Chunyan ;

Muhammad, A. K. M. Ghulam ;

Clark, Mary C. ;

Arditi, Moshe ;

Comin-Anduix, Begonya ;

Ribas, Antoni ;

Lowenstein, Pedro R. ;

Castro, Maria G. .

PLOS MEDICINE, 2009, 6 (01) :83-104

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