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Targeting WEE1 in tumor-associated dendritic cells potentiates antitumor immunity [scRNA-Seq]

ABSTRACT: Targeting WEE1 in tumor-associated dendritic cells potentiates antitumor immunity [scRNA-Seq]

PROVIDER: PRJNA1122520 | ENA |

REPOSITORIES: ENA

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Targeting WEE1 in tumor-associated dendritic cells potentiates antitumor immunity

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Targeting WEE1 in tumor-associated dendritic cells potentiates antitumor immunity

Project description:DNA damage is a prevalent event within the tumor microenvironment, significantly influencing cancer initiation, progression, metastasis, and immune cell functionality. Here, we observed that oxidative stress induces DNA damage in tumor-associated dendritic cells (TADCs), leading to the activation of the serine/threonine kinase WEE1, which facilitates DNA repair. Notably, this DNA damage also acts as a stimulus for DC activation. Pharmacological inhibition of WEE1 activates TADCs via the cGAS/STING pathway, resulting in an enhanced antitumor immune response and improved tumor control. Furthermore, WEE1 inhibition augments the efficacy of DC vaccines and work synergistically with immune checkpoint blockade therapy. These findings underscore the critical role of WEE1-mediated signaling in DNA damage repair in immune cells in the tumor microenvironment, which in turn dampens the antitumor immune response. Thus, targeting WEE1 in DCs presents a promising strategy to enhance DC-mediated T cell activation and improve the effectiveness of cancer immunotherapy strategies.

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Targeting WEE1 in tumor-associated dendritic cells potentiates antitumor immunity [scRNA-Seq]

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YTHDF1 loss in dendritic cells potentiates radiationinduced antitumor immunity via STING-dependent type I IFN production

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Project description:In this project, we transfected MC38 cells with Flag-tagged Mbtps1 or vector control. After that, we performed immunoprecipitation–mass spectrometry analysis to search the interacting proteins of MBTPS1. In our study, We observed that the loss of membrane-bound transcription factor site-1 protease (MBTPS1) in tumor cells enhanced antitumor immunity and potentiated anti-PD-1 therapy. Mechanistic studies revealed that tumor cell-intrinsic MBTPS1 competed with USP13 for binding to STAT1, thereby disrupting USP13-dependent deubiquitination and stabilization of STAT1. MBTPS1 deficiency induced CXCR3+ CD8+ T cell infiltration by upregulating STAT1-transcribed chemokines including CXCL9, CXCL10 and CXCL11. Notably, the regulatory role of MBTPS1 in antitumor immunity operates independently of its classic function in cleaving membrane-bound transcription factors. Collectively, our results provide a theoretical basis for MBTPS1 as a potential immunotherapy target and also as a predictor of immunotherapy efficacy.

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Noncanonical MAVS signaling restrains dendritic cell-driven antitumor immunity by inhibiting IL-12

Project description:MAVS-mediated cytosolic RNA sensing plays a central role in tumor immunogenicity. However, the effects of host MAVS signaling on antitumor immunity remains uncertain. Here, we demonstrate that host MAVS pathway drives accelerated tumor growth and impairs antitumor immunity, while MAVS knockout in dendritic cells (DCs) promotes tumor-reactive CD8+ T cell responses. Specifically, the CD8+ T cell priming capacity is enhanced by lack of functional MAVS in a type I interferon-independent, but IL-12-dependent, manner. Mechanistically, loss of RIG-I/MAVS cascade activates non-canonical NF-κB pathway and in turn induces IL-12 production by DCs, resulting in CD8+ T cell: DC crosstalk licensed by IFN-γ and IL-12. Moreover, ablation of host MAVS sensitizes tumors to immunotherapy and attenuates radiation resistance, thereby facilitating the maintenance of effector CD8+ T cells. These findings identify that host MAVS pathway acts as an immune checkpoint of DC-driven antitumor immunity, indicating the development of DC-based immunotherapies through MAVS signaling antagonism.

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