Abstract
A recent in vitro study showed that pharmacological inhibition of the nuclear export receptor XPO1 suppresses oxaliplatin-induced nuclear release of HMGB1 and HMGB2, as well as the translocation of CALR to the plasma membrane. Moreover, cell-targeted-HMGB2 protein potently induced CALR exposure, even in the absence of oxaliplatin.
Keywords:
Adjuvanticity; Calreticulin; Immunotherapy; checkpoint blockade.
MeSH terms
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Animals
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Antineoplastic Agents / pharmacology
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Calreticulin* / metabolism
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Cytoplasm / metabolism
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Exportin 1 Protein
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HMGB1 Protein / metabolism
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HMGB2 Protein* / genetics
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HMGB2 Protein* / metabolism
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Humans
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Immunogenic Cell Death* / drug effects
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Karyopherins / metabolism
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Oxaliplatin / pharmacology
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Protein Transport
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Receptors, Cytoplasmic and Nuclear / metabolism
Substances
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Calreticulin
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HMGB2 Protein
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HMGB1 Protein
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CALR protein, human
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Karyopherins
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Antineoplastic Agents
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Oxaliplatin
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Exportin 1 Protein
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Receptors, Cytoplasmic and Nuclear