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      Type I interferon induces cancer stem cells-mediated chemotherapy resistance

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      Author(s): a , a , b
      Publication date (Electronic, pub):
      Publication date (Electronic, collection):
      Journal: Oncoimmunology
      Publisher: Taylor & Francis
      Keywords: Chemotherapy, immunogenic cell death, epigenetic immune escape, cancer stem cells, interferon type I, KDM1B

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          ABSTRACT

          In a recent study in Nature Immunology, Musella et al. demonstrate that suboptimal type I interferon (IFN-I) signaling in tumors undergoing immunogenic cell death (ICD) facilitates the accumulation of cancer stem cells (CSCs) by triggering the epigenetic regulator lysine demethylase 1B (KDM1B). KDM1B stands out as a promising target for the development of novel strategies to improve anti-cancer responses driven by ICD.

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          Cancer cell-autonomous contribution of type I interferon signaling to the efficacy of chemotherapy.

          Antonella Sistigu, Takahiro Yamazaki, Erika Vacchelli … (2014)
          Some of the anti-neoplastic effects of anthracyclines in mice originate from the induction of innate and T cell-mediated anticancer immune responses. Here we demonstrate that anthracyclines stimulate the rapid production of type I interferons (IFNs) by malignant cells after activation of the endosomal pattern recognition receptor Toll-like receptor 3 (TLR3). By binding to IFN-α and IFN-β receptors (IFNARs) on neoplastic cells, type I IFNs trigger autocrine and paracrine circuitries that result in the release of chemokine (C-X-C motif) ligand 10 (CXCL10). Tumors lacking Tlr3 or Ifnar failed to respond to chemotherapy unless type I IFN or Cxcl10, respectively, was artificially supplied. Moreover, a type I IFN-related signature predicted clinical responses to anthracycline-based chemotherapy in several independent cohorts of patients with breast carcinoma characterized by poor prognosis. Our data suggest that anthracycline-mediated immune responses mimic those induced by viral pathogens. We surmise that such 'viral mimicry' constitutes a hallmark of successful chemotherapy.
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            Mitochondrial DNA drives abscopal responses to radiation that are inhibited by autophagy

            Takahiro Yamazaki, Alexander Kirchmair, Ai Sato … (2020)
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              Apoptotic caspases inhibit abscopal responses to radiation and identify a new prognostic biomarker for breast cancer patients

              María Esperanza Rodríguez-Ruiz, Aitziber Buqué, Michal Hensler … (2019)
              Caspase 3 (CASP3) has a key role in the execution of apoptosis, and many cancer cells are believed to disable CASP3 as a mechanism of resistance to cytotoxic therapeutics. Alongside, CASP3 regulates stress-responsive immunomodulatory pathways, including secretion of type I interferon (IFN). Here, we report that mouse mammary carcinoma TSA cells lacking Casp3 or subjected to chemical caspase inhibition were as sensitive to the cytostatic and cytotoxic effects of radiation therapy (RT) in vitro as their control counterparts, yet secreted increased levels of type I IFN. This effect originated from the accrued accumulation of irradiated cells with cytosolic DNA, likely reflecting the delayed breakdown of cells experiencing mitochondrial permeabilization in the absence of CASP3. Casp3 -/- TSA cells growing in immunocompetent syngeneic mice were more sensitive to RT than their CASP3-proficient counterparts, and superior at generating bona fide abscopal responses in the presence of an immune checkpoint blocker. Finally, multiple genetic signatures of apoptotic proficiency were unexpectedly found to have robust negative (rather than positive) prognostic significance in a public cohort of breast cancer patients. However, these latter findings were not consistent with genetic signatures of defective type I IFN signaling, which were rather associated with improved prognosis. Differential gene expression analysis on patient subgroups with divergent prognosis (as stratified by independent signatures of apoptotic proficiency) identified SLC7A2 as a new biomarker with independent prognostic value in breast cancer patients. With the caveats associated with the retrospective investigation of heterogeneous, public databases, our data suggest that apoptotic caspases may influence the survival of breast cancer patients (or at least some subsets thereof) via mechanisms not necessarily related to type I IFN signaling as they identify a novel independent prognostic biomarker that awaits prospective validation.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Oncoimmunology
                Journal ID (iso-abbrev): Oncoimmunology
                Title: Oncoimmunology
                Publisher: Taylor & Francis
                ISSN (Print): 2162-4011
                ISSN (Electronic): 2162-402X
                Publication date (Electronic, pub): 22 September 2022
                Publication date (Electronic, collection): 2022
                Publication date PMC-release: 22 September 2022
                Volume: 11
                Issue: 1
                Electronic Location Identifier: 2127274
                Affiliations
                [a ]Department of Radiation Oncology, Weill Cornell Medical College; , New York, NY, USA
                [b ]Sandra and Edward Meyer Cancer Center; , New York, NY, USA
                Author notes
                CONTACT Claire Vanpouille-Box clv2002@ 123456med.cornell.edu Weill Cornell Medical College; , Stich Radiation Oncology, 525 East 68th Street, Box #169, New York, NY 10065, USA
                Author information
                https://orcid.org/0000-0001-7213-0670
                Article
                Publisher ID: 2127274
                DOI: 10.1080/2162402X.2022.2127274
                PMC ID: 9518997
                PubMed ID: 36185803
                SO-VID: b9c9114a-76b7-4a68-a3e3-0e708564aaeb
                Copyright © © 2022 The Author(s). Published with license by Taylor & Francis Group, LLC.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License ( http://creativecommons.org/licenses/by-nc/4.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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                Page count
                Figures: 1, References: 10, Pages: 1
                Categories
                Subject: Article Commentary
                Subject: Commentary

                ScienceOpen disciplines: Immunology
                Keywords: chemotherapy,immunogenic cell death,epigenetic immune escape,cancer stem cells,interferon type i,kdm1b
                Data availability:
                ScienceOpen disciplines: Immunology
                Keywords: chemotherapy, immunogenic cell death, epigenetic immune escape, cancer stem cells, interferon type i, kdm1b

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