ArticleCancer research2020
FIP200 Suppresses Immune Checkpoint Therapy Responses in Breast Cancers by Limiting AZI2/TBK1/IRF Signaling Independent of Its Canonical Autophagy Function.
Article in Cancer research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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27 citing papers in PubMed, 37 citations in OpenAlex.
- NAP1 switches from an activator to a limiter of interferon induction by trapping TBK1 in condensates.Nature communications · 2026Article
- Machine learning-based predictive models and subtypes patterns in peripheral blood of schizophrenia based on a machine learning computational framework.Schizophrenia (Heidelberg, Germany) · 2026Article
- FIP200 regulates plasma B cell differentiation via mitochondrial and heme homeostasis.The Journal of experimental medicine · 2026Article
- Cell death and immune escape in the tumor microenvironment: associated mechanisms, opportunities and challenges.Apoptosis : an international journal on programmed cell death · 2026Review
- Attack cancer: Through autophagic modulations as suppressor or promoter.World journal of clinical oncology · 2025Review
- An RB1CC1 Missense Variant in Nova Scotia Duck Tolling Retrievers with Degenerative Encephalopathy.Genes · 2025Article
- Daurisoline Modulates the TBK1-Dependent Type I Interferon Pathway to Boost Anti-tumor Immunity via Targeting of LRP1.Research (Washington, D.C.) · 2025Article
- Role of Tumor Cell Intrinsic and Host Autophagy in Cancer.Cold Spring Harbor perspectives in medicine · 2024Review
- Beyond self‑eating: Emerging autophagy‑independent functions for the autophagy molecules in cancer (Review).International journal of oncology · 2024Review
- Role of NuMA1 in breast cancer stem cells with implications for combination therapy of PIM1 and autophagy inhibition in triple negative breast cancer.Research square · 2024Article
- Article
- TBK1 is paradoxical in tumor development: a focus on the pathway mediating IFN-I expression.Frontiers in immunology · 2024Review
- Autophagy-amplifying nanoparticles evoke immunogenic cell death combined with anti-PD-1/PD-L1 for residual tumors immunotherapy after RFA.Journal of nanobiotechnology · 2023Article
- Autophagy and autophagy-related pathways in cancer.Nature reviews. Molecular cell biology · 2023Review
- Regulation of RB1CC1/FIP200 stability and autophagy function by CREBBP-mediated acetylation in an intrinsically disordered region.Autophagy · 2023Article
- Impact of context-dependent autophagy states on tumor progression.Nature cancer · 2023Review
- Autophagy inhibition prevents lymphatic malformation progression to lymphangiosarcoma by decreasing osteopontin and Stat3 signaling.Nature communications · 2023Article
- Autophagy and tumorigenesis.The FEBS journal · 2022Review
- TRIM27 cooperates with STK38L to inhibit ULK1-mediated autophagy and promote tumorigenesis.The EMBO journal · 2022Article
- Biglycan Promotes Cancer Stem Cell Properties, NFκB Signaling and Metastatic Potential in Breast Cancer Cells.Cancers · 2022Article
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7 authors at 2 institutions in 2 countries.
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Abstract
Immune checkpoint inhibitors (ICI) have the potential to induce durable therapeutic responses, yet response rates in breast cancer are modest and limited to particular subtypes. To expand the applicability of ICI, we examined the role of an essential autophagy gene, FIP200, which has been shown to be important for tumor progression in mammary tumors. Specific disruption of the autophagy function of FIP200 or complete ablation of FIP200 in genetic mouse models revealed that FIP200 autophagy function was required for progression of PyMT-driven mammary tumors. However, a noncanonical autophagy function of FIP200 was responsible for limiting T-cell recruitment and activation of the TBK1-IFN signaling axis. FIP200 also interacted with the TBK1 adaptor protein, AZI2, which was crucial for activation of TBK1 following FIP200 ablation. Accordingly, disrupting the noncanonical autophagy function of FIP200 in combination with ICI therapy led to superior, durable responses in immune-competent models of breast cancer. Collectively, these insights could guide future development of therapeutic agents against FIP200 for combinatorial ICI therapies in nonresponsive breast cancers. SIGNIFICANCE: These findings show that deletion of FIP200 enhances immune checkpoint inhibitor efficacy in nonresponsive breast cancer.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.