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Hayashi, K; Nikolos, F; Lee, Y C; Jain, A; Tsouko, E; Gao, H; Kasabyan, A; Leung, H E; Osipov, A; Jung, S Y; Kurtova, A V; Chan, K S
Nature communications, 12/2020, Volume: 11, Issue: 1Journal Article
Induction of tumor cell death is the therapeutic goal for most anticancer drugs. Yet, a mode of drug-induced cell death, known as immunogenic cell death (ICD), can propagate antitumoral immunity to augment therapeutic efficacy. Currently, the molecular hallmark of ICD features the release of damage-associated molecular patterns (DAMPs) by dying cancer cells. Here, we show that gemcitabine, a standard chemotherapy for various solid tumors, triggers hallmark immunostimualtory DAMP release (e.g., calreticulin, HSP70, and HMGB1); however, is unable to induce ICD. Mechanistic studies reveal gemcitabine concurrently triggers prostaglandin E release as an inhibitory DAMP to counterpoise the adjuvanticity of immunostimulatory DAMPs. Pharmacological blockade of prostaglandin E biosythesis favors CD103 dendritic cell activation that primes a Tc1-polarized CD8 T cell response to bolster tumor rejection. Herein, we postulate that an intricate balance between immunostimulatory and inhibitory DAMPs could determine the outcome of drug-induced ICD and pose COX-2/prostaglandin E blockade as a strategy to harness ICD.
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