The co-translocation of ERp57 and calreticulin determines the immunogenicity of cell death

被引:0
|
作者
T Panaretakis
N Joza
N Modjtahedi
A Tesniere
I Vitale
M Durchschlag
G M Fimia
O Kepp
M Piacentini
K-U Froehlich
P van Endert
L Zitvogel
F Madeo
G Kroemer
机构
[1] INSERM,Department of Biology
[2] Unit 848 ‘Apoptosis,undefined
[3] Cancer and Immunity’,undefined
[4] Institut Gustave Roussy,undefined
[5] Faculté Paris Sud-Université Paris 11,undefined
[6] Institute of Molecular Biosciences,undefined
[7] Universitaetsplatz 2,undefined
[8] University of Graz,undefined
[9] National Institute for Infectious Diseases ‘Lazzaro Spallanzani’,undefined
[10] University of Rome ‘Tor Vergata’,undefined
[11] INSERM,undefined
[12] U580,undefined
[13] Faculté de Médecine René Descartes,undefined
[14] Université Paris-Descartes,undefined
[15] INSERM,undefined
[16] U805,undefined
[17] Institut Gustave Roussy,undefined
来源
Cell Death & Differentiation | 2008年 / 15卷
关键词
apoptosis; endoplasmic reticulum; anthracyclines;
D O I
暂无
中图分类号
学科分类号
摘要
The exposure of calreticulin (CRT) on the plasma membrane can precede anthracycline-induced apoptosis and is required for cell death to be perceived as immunogenic. Mass spectroscopy, immunofluorescence and immunoprecipitation experiments revealed that CRT co-translocates to the surface with another endoplasmic reticulum-sessile protein, the disulfide isomerase ERp57. The knockout and knockdown of CRT or ERp57 inhibited the anthracycline-induced translocation of ERp57 or CRT, respectively. CRT point mutants that fail to interact with ERp57 were unable to restore ERp57 translocation upon transfection into crt−/− cells, underscoring that a direct interaction between CRT and ERp57 is strictly required for their co-translocation to the surface. ERp57low tumor cells generated by retroviral introduction of an ERp57-specific shRNA exhibited a normal apoptotic response to anthracyclines in vitro, yet were resistant to anthracycline treatment in vivo. Moreover, ERp57low cancer cells (which failed to expose CRT) treated with anthracyclines were unable to elicit an anti-tumor response in conditions in which control cells were highly immunogenic. The failure of ERp57low cells to elicit immune responses and to respond to chemotherapy could be overcome by exogenous supply of recombinant CRT protein. These results indicate that tumors that possess an intrinsic defect in the CRT-translocating machinery become resistant to anthracycline chemotherapy due to their incapacity to elicit an anti-cancer immune response.
引用
收藏
页码:1499 / 1509
页数:10
相关论文
共 50 条
  • [41] Upregulation of ERp57 promotes clear cell renal cell carcinoma progression by initiating a STAT3/ILF3 feedback loop
    Liu, Yan
    Wang, Jian-Xing
    Nie, Zi-Yuan
    Wen, Yue
    Jia, Xin-Ju
    Zhang, Li-Na
    Duan, Hui-Jun
    Shi, Yong-Hong
    JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH, 2019, 38 (01)
  • [42] Upregulation of ERp57 promotes clear cell renal cell carcinoma progression by initiating a STAT3/ILF3 feedback loop
    Yan Liu
    Jian-Xing Wang
    Zi-Yuan Nie
    Yue Wen
    Xin-Ju Jia
    Li-Na Zhang
    Hui-Jun Duan
    Yong-Hong Shi
    Journal of Experimental & Clinical Cancer Research, 38
  • [43] Off-the-shelf CAR-NK cells targeting immunogenic cell death marker ERp57 execute robust antitumor activity and have a synergistic effect with ICD inducer oxaliplatin
    Zheng, Liuhai
    Wang, Huifang
    Zhou, Jihao
    Shi, Guangwei
    Ma, Jingbo
    Jiang, Yuke
    Dong, Zhiyu
    Li, Jiexuan
    He, Yuan-Qiao
    Wu, Dinglan
    Sun, Jichao
    Xu, Chengchao
    Li, Zhijie
    Wang, Jigang
    JOURNAL FOR IMMUNOTHERAPY OF CANCER, 2024, 12 (07)
  • [44] The role of ERp57 in disulfide bond formation during the assembly of major histocompatibility complex class I in a synchronized semipermeabilized cell translation system
    Farmery, MR
    Allen, S
    Allen, AJ
    Bulleid, NJ
    JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (20) : 14933 - 14938
  • [45] Intestinal Cell Phosphate Uptake and the Targeted Knockout of the 1,25D3-MARRS Receptor/PDIA3/ERp57
    Nemere, Ilka
    Garcia-Garbi, Natalio
    Haemmerling, Guenter J.
    Winger, Quinton
    ENDOCRINOLOGY, 2012, 153 (04) : 1609 - 1615
  • [46] Intestinal Cell Calcium Uptake and the Targeted Knockout Of the 1,25D3-MARRS Receptor/PDIA3/Erp57
    Nemere, Ilka
    Garbi, Natalio
    Hammerling, Gunter
    FASEB JOURNAL, 2010, 24
  • [47] The ERp57/GRp58/1,25D3-MARRS receptor:: Multiple functional roles in diverse cell systems
    Khanal, R. C.
    Nemere, I.
    CURRENT MEDICINAL CHEMISTRY, 2007, 14 (10) : 1087 - 1093
  • [48] HMGB2-induced calreticulin translocation required for immunogenic cell death and ferroptosis of cancer cells are controlled by the nuclear exporter XPO1
    Fan, Jingqi
    Gillespie, Kevin P.
    Mesaros, Clementina
    Blair, Ian A.
    COMMUNICATIONS BIOLOGY, 2024, 7 (01)
  • [49] Co-activation of synaptic and extrasynaptic NMDA receptors by neuronal insults determines cell death in acute brain slice
    Chen, Zhuoyou
    Zhou, Quan
    Zhang, Min
    Wang, Hongbing
    Yun, Weiwen
    Zhou, Xianju
    NEUROCHEMISTRY INTERNATIONAL, 2014, 78 : 28 - 34
  • [50] Comparative Proteomic Analysis of Paclitaxel Sensitive A2780 Epithelial Ovarian Cancer Cell Line and Its Resistant Counterpart A2780TC1 by 2D-DIGE: The Role of ERp57
    Cicchillitti, Lucia
    Di Michele, Michela
    Urbani, Andrea
    Ferlini, Cristiano
    Donati, Maria Benedetta
    Scambia, Giovanni
    Rotilio, Domenico
    JOURNAL OF PROTEOME RESEARCH, 2009, 8 (04) : 1902 - 1912