Sequential Interferon β-Cisplatin Treatment Enhances the Surface Exposure of Calreticulin in Cancer Cells via an Interferon Regulatory Factor 1-Dependent Manner.
Calreticulin
/ metabolism
Cell Line, Tumor
Cell Survival
/ drug effects
Cisplatin
/ pharmacology
Doxorubicin
/ pharmacology
Humans
Immunogenic Cell Death
/ drug effects
Interferon Regulatory Factor-1
/ metabolism
Interferon-beta
/ pharmacology
Oxaliplatin
/ pharmacology
Proto-Oncogene Proteins c-jun
/ metabolism
bioinformatics
chemotherapy
endoplasmic reticulum stress
immunogenic cell death
interferon
Journal
Biomolecules
ISSN: 2218-273X
Titre abrégé: Biomolecules
Pays: Switzerland
ID NLM: 101596414
Informations de publication
Date de publication:
21 04 2020
21 04 2020
Historique:
received:
01
04
2020
revised:
14
04
2020
accepted:
18
04
2020
entrez:
25
4
2020
pubmed:
25
4
2020
medline:
7
4
2021
Statut:
epublish
Résumé
Immunogenic cell death (ICD) refers to a unique form of cell death that activates an adaptive immune response against dead-cell-associated antigens. Accumulating evidence indicates that the efficacy of conventional anticancer agents relies on not only their direct cytostatic/cytotoxic effects but also the activation of antitumor ICD. Common anticancer ICD inducers include certain chemotherapeutic agents (such as anthracyclines, oxaliplatin, and bortezomib), radiotherapy, photodynamic therapy (PDT), and oncolytic virotherapies. However, most chemotherapeutic reagents are inefficient or fail to trigger ICD. Therefore, better understanding on the molecular determinants of chemotherapy-induced ICD will help in the development of more efficient combinational anticancer strategies through converting non- or relatively weak ICD inducers into bona fide ICD inducers. In this study, we found that sequential, but not concurrent, treatment of cancer cells with interferon β (IFNβ), a type I IFN, and cisplatin (an inefficient ICD inducer) can enhance the expression of ICD biomarkers in cancer cells, including surface translocation of an endoplasmic reticulum (ER) chaperone, calreticulin (CRT), and phosphorylation of the eukaryotic translation initiation factor alpha (eIF2α). These results suggest that exogenous IFNβ may activate molecular determinants that convert cisplatin into an ICD inducer. Further bioinformatics and in vitro experimental analyses found that interferon regulatory factor 1 (IRF1) acted as an essential mediator of surface CRT exposure by sequential IFNβ-cisplatin combination. Our findings not only help to design more effective combinational anticancer therapy using IFNβ and cisplatin, but also provide a novel insight into the role of IRF1 in connecting the type I IFN responses and ICD.
Identifiants
pubmed: 32326356
pii: biom10040643
doi: 10.3390/biom10040643
pmc: PMC7226424
pii:
doi:
Substances chimiques
Calreticulin
0
Interferon Regulatory Factor-1
0
Proto-Oncogene Proteins c-jun
0
Oxaliplatin
04ZR38536J
Interferon-beta
77238-31-4
Doxorubicin
80168379AG
Cisplatin
Q20Q21Q62J
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NCI NIH HHS
ID : P50 CA098252
Pays : United States
Organisme : Ministry of Science and Technology, Taiwan
ID : MOST108-2314-B-038-010
Pays : International
Organisme : Health and welfare surcharge of tobacco products
ID : MOHW109-TDU-B-212-134020
Pays : International
Organisme : Ministry of Education
ID : DP2-108-21121-01-C-03-05
Pays : International
Déclaration de conflit d'intérêts
The authors declare no conflict of interest.
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