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HMGB1-induced autophagy promotes chemotherapy resistance in leukemia cells.

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WOS被引频次:137
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成果类型:
期刊论文
作者:
Liu, L.;Yang, M.;Kang, R.;Wang, Z.;Zhao, Y.;Yu, Y.;Xie, M.;Yin, X.;Livesey, K. M.;Lotze, M. T.;Tang, D.;Cao, L.
通讯作者:
Cao, L
作者机构:
[Cao, L.; Xie, M.; Zhao, Y.; Wang, Z.; Yang, M.; Kang, R.; Liu, L.; Yu, Y.] Cent S Univ, Dept Pediat, Xiangya Hosp, Changsha 410008, Hunan, Peoples R China.
[Livesey, K. M.; Lotze, M. T.; Tang, D.] Univ Pittsburgh, Dept Surg, Hillman Canc Ctr, Inst Canc, Pittsburgh, PA USA.
[Yin, X.] Nanhua Univ, Affiliated Hosp 1, Dept Pediat, Hengyang, Hunan, Peoples R China.
通讯机构:
[Cao, L] Cent S Univ, Dept Pediat, Xiangya Hosp, 110 Xiangya Rd Changsha, Changsha 410008, Hunan, Peoples R China.
语种:
英文
关键词:
HMGB1;autophagy;PI3K;ERK;drug resistance
期刊:
Leukemia
ISSN:
0887-6924
年:
2011
卷:
25
期:
1
页码:
23-31
文献类别:
WOS:Article
所属学科:
ESI学科类别:临床医学;WOS学科类别:Hematology;Oncology
入藏号:
WOS:000286179400003;PMID:20927132
基金类别:
National Natural Sciences Foundation of China [30571982, 30772353, 30973234, 30500485]; Doctoral Program of Higher Education of China [20070533042]; University of Pittsburgh
机构署名:
本校为其他机构
摘要:
Autophagy, a tightly regulated lysosome-dependent catabolic pathway, is important in the regulation of cancer development and progression and in determining the response of tumor cells to anticancer therapy. However, the role of autophagy in leukemia still remains largely unknown. Here we show that high-mobility group box 1 (HMGB1), the best characterized damage-associated molecular pattern, was released from leukemia cell lines after chemotherapy-induced cytotoxicity and activated autophagy to protect against injury. Treatment with HMGB1-neutralizing antibodies increased the sensitivity of leukemia cells to chemotherapy; whereas, exogenous HMGB1 rendered these cells more resistant to drug-induced cytotoxicity. Moreover, exogenous HMGB1 increased autophagy as evaluated by increased expression of the autophagic marker microtubule-associated protein light chain 3-II, degradation of sequestosome 1 (p62) and autophagosome formation. Furthermore, knockdown or pharmacological inhibition of either phosphoinositide 3-kinase-III or extracellular signal-regulated kinase kinase mitogen-activated protein kinase kinase/extra-cellular signal-regulated protein kinase inhibited HMGB1-induced autophagy. Taken together, these results suggest that HMGB1 release after chemotherapy is a critical regulator of autophagy and a potential drug target for therapeutic interventions in leukemia. Leukemia (2011) 25, 23-31; doi: 10.1038/leu.2010.225; published online 7 October 2010
参考文献:
Tang DL, 2007, J LEUKOCYTE BIOL, V81, P741, DOI 10.1189/jlb.0806540
Wang JR, 2009, J BIOL CHEM, V284, P21412, DOI 10.1074/jbc.M109.026013
Pankiv S, 2007, J BIOL CHEM, V282, P24131, DOI 10.1074/jbc.M702824200
Davies CC, 2004, J BIOL CHEM, V279, P1010, DOI 10.1074/jbc.M303820200
Tang DL, 2010, BBA-GENE REGUL MECH, V1799, P131, DOI 10.1016/j.bbagrm.2009.11.014

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