The histone deacetylase inhibitor vorinostat induces calreticulin exposure in childhood brain tumour cells in vitro
Author(s) -
Jürgen Sonnemann,
Stephanie Greßmann,
Jonathan Becker,
Susan Wittig,
Mareike Schmudde,
James F. Beck
Publication year - 2010
Publication title -
cancer chemotherapy and pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.112
H-Index - 111
eISSN - 1432-0843
pISSN - 0344-5704
DOI - 10.1007/s00280-010-1302-4
Subject(s) - vorinostat , histone deacetylase inhibitor , cancer research , calreticulin , histone deacetylase , immunogenic cell death , biology , camptothecin , apoptosis , pharmacology , programmed cell death , microbiology and biotechnology , histone , endoplasmic reticulum , biochemistry , gene
It has recently been recognised that anticancer chemotherapy can elicit an immunogenic form of apoptosis characterised by the exposure of calreticulin (CRT) on the surface of dying tumour cells, entailing an immune response that contributes to the therapeutic outcome. CRT exposure has been found to be induced by anthracyclins and oxaliplatin, but not by other proapoptotic antineoplastic agents including etoposide, camptothecin and cisplatin. In this study, we examined the histone deacetylase inhibitor vorinostat for its capability to stimulate CRT exposure in tumour cells.
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