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Induction of immunogenic cell death of tumors by newly synthesized heterocyclic quinone derivative

Title
Induction of immunogenic cell death of tumors by newly synthesized heterocyclic quinone derivative
Authors
Son, Keum-jooChoi, Ki RyungRyu, Chung-KyuLee, Seog JaeKim, Ho JeongLee, Hyunah
Ewha Authors
유충규김호정
SCOPUS Author ID
유충규scopus; 김호정scopus
Issue Date
2017
Journal Title
PLOS ONE
ISSN
1932-6203JCR Link
Citation
vol. 12, no. 3
Publisher
PUBLIC LIBRARY SCIENCE
Indexed
SCIE; SCOPUS WOS
Abstract
Many cancer types are serious diseases causing mortality, and new therapeutics with improved efficacy and safety are required. Immuno-(cell)-therapy is considered as one of the promising therapeutic strategies for curing intractable cancer. In this study, we tested R2016, a newly developed heterocyclic quinone derivative, for induction of immunogenic tumor cell death and as a possible novel immunochemotherapeutic. We studied the anticancer effects of R2016 against LLC, a lung cancer cell line and B16F10, a melanoma cell line. LLC (non-immunogenic) and B16F10 (immunogenic) cells were killed by R2016 in dose-dependent manner. R2016 reduced the viability of both LLC and B16F10 tumor cells by inducing apoptosis and necrosis, while it demonstrated no cytotoxicity against normal splenocytes. Expression of immunogenic death markers on the cell surface of R2016 treated tumor cells including calreticulin (CRT) and heat shock proteins (HSPs) was increased along with the induction of their genes. Increased CRT expression correlated with dendritic cell (DC) uptake of dying tumor cells: the proportion of CRT(+)CD11c(+)cells was increased in the R2016-treated group. The gene transcription of Calr3, Hspb1, and Tnfaip6, which are related to immunogenicity induction of dead cells, was up-regulated in the R2016 treated tumor cells. On the other hand, ANGPT1, FGF7, and URGCP gene levels were down-regulated by R2016 treatment. This data suggests that R2016 induced immunogenic tumor cell death, and suggests R2016 as an effective anti-tumor immunochemotherapeutic modality.
DOI
10.1371/journal.pone.0173121
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약학대학 > 약학과 > Journal papers
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