ArticleCancer immunology, immunotherapy : CII2023
Mitochondrial C1QBP is essential for T cell antitumor function by maintaining mitochondrial plasticity and metabolic fitness.
Article in Cancer immunology, immunotherapy : CII, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- Cyclophilin D reduces Ca2+ sequestration by complement 1q binding protein.The Biochemical journal · 2025Article
- Trace element-dictated exosome modules and self-adaptive dual-network hydrogel orchestrate diabetic foot regeneration through complement-mitochondria-autophagy circuitry.Military Medical Research · 2025Article
- PA28γ promotes the malignant progression of tumor by elevating mitochondrial function via C1QBP.eLife · 2025Article
- Advances in strategies to improve the immunotherapeutic efficacy of chimeric antigen receptor-T cell therapy for lymphoma.Cancer biology & medicine · 2025Review
- Integrative pan-cancer genomic analysis highlights mitochondrial protein p32 as a potential therapeutic target in Myc-driven tumorigenesis.Medical oncology (Northwood, London, England) · 2025Article
- Role of PGC-1α in the proliferation and metastasis of malignant tumors.Journal of molecular histology · 2025Review
- Novel cuproptosis-related genesOpen life sciences · 2025Article
- Targeting mitochondria: restoring the antitumor efficacy of exhausted T cells.Molecular cancer · 2024Review
- Pan-cancer analysis implicates novel insights of lactate metabolism into immunotherapy response prediction and survival prognostication.Journal of experimental & clinical cancer research : CR · 2024Article
- Impact of mitochondrial dysfunction on the antitumor effects of immune cells.Frontiers in immunology · 2024Review
- Macrophages Promote Atherosclerosis Development by Inhibiting CD8T Cell Apoptosis.Mediators of inflammation · 2024Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The metabolic stress present in the tumor microenvironment of many cancers can attenuate T cell antitumor activity, which is intrinsically controlled by the mitochondrial plasticity, dynamics, metabolism, and biogenesis within these T cells. Previous studies have reported that the complement C1q binding protein (C1QBP), a mitochondrial protein, is responsible for maintenance of mitochondrial fitness in tumor cells; however, its role in T cell mitochondrial function, particularly in the context of an antitumor response, remains unclear. Here, we show that C1QBP is indispensable for T cell antitumor immunity by maintaining mitochondrial integrity and homeostasis. This effect holds even when only one allele of C1qbp is functional. Further analysis of C1QBP in the context of chimeric antigen receptor (CAR) T cell therapy against the murine B16 melanoma model confirmed the cell-intrinsic role of C1QBP in regulating the antitumor functions of CAR T cells. Mechanistically, we found that C1qbp knocking down impacted mitochondrial biogenesis via the AMP-activated protein kinase (AMPK)/peroxisome proliferator-activated receptor gamma coactivator 1-alpha signaling pathway, as well as mitochondrial morphology via the phosphorylation of mitochondrial dynamics protein dynamin-related protein 1. In summary, our study provides a novel mitochondrial target to potentiate the plasticity and metabolic fitness of mitochondria within T cells, thus improving the immunotherapeutic potential of these T cells against tumors.
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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.