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Temozolomide increases MHC‐I expression via NF‐κB signaling in glioma stem cells
Author(s) -
Zhang Dongyong,
Qiu Bo,
Wang Yunjie,
Guan Yanlei,
Zhang Luyang,
Wu Anhua
Publication year - 2017
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.10773
Subject(s) - temozolomide , glioma , cancer research , nf κb , chemistry , stem cell , signal transduction , microbiology and biotechnology , biology
Gliomas are the most common and primary tumors of the central nervous system in adults. Temozolomide (TMZ) is the main drug used to treat glioma; however, prognosis remains poor for most patients. Glioma stem cells (GSCs) are thought to enable glioma initiation and evasion from immune surveillance; their immunogenicity can be determined by expression of major histocompatibility complex (MHC)‐I. The present study investigated the effect of TMZ on MHC‐I expression in GSCs. Glioma spheres were cultured in serum‐free medium containing epidermal growth factor, basic fibroblast growth factor, and B27; MHC‐I expression was detected by immunocytochemistry, quantitative real‐time PCR, and flow cytometry. Nuclear factor (NF)‐κB expression in glioma stem cells was detected by Western blot. TMZ enhanced MHC‐I expression in GSCs, and NF‐κB was activated. TMZ treatment increased MHC‐I expression via modulation of NF‐κB signaling in GSCs. In addition to being a chemotherapeutic agent, TMZ may also serve as an immunomodulatory agent in the treatment of glioma patients.