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KDM1B is an important regulator of cytokine signaling in the tumor immune microenvironment and response to immune checkpoint therapy (ChIP-seq)

ABSTRACT: KDM1B is an important regulator of cytokine signaling in the tumor immune microenvironment and response to immune checkpoint therapy (ChIP-seq)

PROVIDER: PRJNA558501 | ENA |

REPOSITORIES: ENA

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KDM1B is an important regulator of cytokine signaling in the tumor immune microenvironment and response to immune checkpoint therapy (ChIP-seq)

Project description:Tumor microenvironment (TME) plays an important role in immune evasion and resistance to immune checkpoint therapy. Here, by using genetic, epigenetic, tumor biology and immunology approaches, we unraveled a key function of KDM1B in TME. KDM1B is important for maintaining several pro-oncogenic cytokine/chemokine signaling pathways. In vivo in resistant and inflammatory breast cancer models, ablation of KDM1B in tumor cells results in increased T cell activity and significantly improved response to anti-PD-1/anti-CTLA-4 therapy. Thus, this study identifies KDM1B as a key regulator of tumor immune microenvironment and offered the mechanistical basis for using KDM1B inhibitors in combinatory therapy to overcome resistance to immune checkpoint blockade.

2021-06-01 | GSE135344 | GEO

KDM1B is an important regulator of cytokine signaling in the tumor immune microenvironment and response to immune checkpoint therapy (RNA-seq)

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KDM1B is an important regulator of cytokine signaling in the tumor immune microenvironment and response to immune checkpoint therapy (RNA-seq)

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Type I IFNs promote cancer cell stemness by triggering the epigenetic regulator KDM1B

Project description:Cancer stem cells (CSCs) are immature, immortal cells within tumors, adept at resisting therapeutic pressure and responsible for local and distant disease recurrence. Non-genetic mechanisms of acquired resistance are increasingly being described, however molecular insights into this evolutionary process still lack. Here, we showed that Type I interferons (IFNs-I) act as molecular hubs of resistance during immunogenic chemotherapy, as they trigger the epigenetic regulator KDM1B, responsible for an adaptive, yet reversible, transcriptional rewiring of cancer cells towards stemness and immune escape. Accordingly, KDM1B pharmacological inhibition antagonizes the appearance of IFN-I-adapted CSCs, both in vitro and in vivo. Notably, IFN-I-adapted CSCs are heterogeneous in terms of multidrug resistance, plasticity, invasiveness and immunogenicity. Moreover, in breast cancer patients receiving anthracycline-based chemotherapy, IFN-I and KDM1B signatures positively correlate with CSC and immune evasion markers. Our study identifies IFN-I→KDM1B axis as a potent engine of cancer cell reprogramming and recommends KDM1B targeting an attractive adjunctive to immunogenic drugs to prevent CSC expansion and increase the long-term benefit of therapy.

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Expression data for KDM1B knockdown in Glioma-Initiating Cells (GICs)

Project description:Glioblastoma (GBM) is the most common and aggressive primary brain tumor in adults, with glioma initiating cells (GICs) implicated to be critical for tumor progression and resistance to therapy. KDM1B is involved in regulating GICs' responses to hypoxia, since over-expression of KDM1B delays the cell growth under hypoxia while knocking-down of KDM1B in GICs promotes their survival and tumorigenic abilities.

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