ArticleJournal for immunotherapy of cancer2022
Mitoribosomal defects aggravate liver cancer via aberrant glycolytic flux and T cell exhaustion.
Article in Journal for immunotherapy of cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 38 citations in OpenAlex.
- Review
- T Cell Exhaustion in Cancer Immunotherapy: Heterogeneity, Mechanisms, and Therapeutic Opportunities.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- T Cell Exhaustion in Hepatocellular Carcinoma: A Substantial Barrier in Immunotherapy.Journal of cellular and molecular medicine · 2026Review
- Metabolic reprogramming-driven resistance to multi-kinase inhibitors in hepatocellular carcinoma: molecular mechanisms and therapeutic opportunities.Molecular cancer · 2026Review
- Mitochondria-related genes or proteins affect the progression of hepatocellular carcinoma: roles, mechanisms and potential treatments.American journal of cancer research · 2026Review
- MRPL37 promotes hepatocellular carcinoma progression through modulating mitochondrial energy metabolism.iScience · 2025Article
- Red ginseng extract enhances mitochondrial function and alleviates immunosenescence in T cells.Journal of ginseng research · 2025Article
- Immunometabolic Targets in CD8Liver cancer · 2025Review
- New insights into T cell metabolism in liver cancer: from mechanism to therapy.Cell death discovery · 2025Review
- Bioinformatics analysis of mitochondrial metabolism-related genes demonstrates their importance in renal cell carcinoma.Discover oncology · 2025Article
- Multimodal cell-cell communication driving CD8Frontiers in immunology · 2025Review
- Mitochondrial ribosomal proteins: potential targets for cancer prognosis and therapy.Frontiers in oncology · 2025Review
- Mitochondria in tumor immune surveillance and tumor therapies targeting mitochondria.Cellular oncology (Dordrecht, Netherlands) · 2024Review
- Co-regulation and synteny of GFM2 and NSA2 links ribosomal function in mitochondria and the cytosol with chronic kidney disease.Molecular medicine (Cambridge, Mass.) · 2024Review
- Cellular senescence and metabolic reprogramming: Unraveling the intricate crosstalk in the immunosuppressive tumor microenvironment.Cancer communications (London, England) · 2024Review
- Elucidating the role of S100A10 in CD8Cell death & disease · 2024Article
- DAP3 promotes mitochondrial activity and tumour progression in hepatocellular carcinoma by regulating MT-ND5 expression.Cell death & disease · 2024Article
- Harnessing CD8Clinical and translational medicine · 2024Review
- Unlocking the potential of T-cell metabolism reprogramming: Advancing single-cell approaches for precision immunotherapy in tumour immunity.Clinical and translational medicine · 2024Review
- Metabolic reprogramming in the tumor microenvironment of liver cancer.Journal of hematology & oncology · 2024Review
Corrections and comments
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Authors and funding
18 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMitochondria are involved in cancer energy metabolism, although the mechanisms underlying the involvement of mitoribosomal dysfunction in hepatocellular carcinoma (HCC) remain poorly understood. Here, we investigated the effects of mitoribosomal impairment-mediated alterations on the immunometabolic characteristics of liver cancer.
methodsWe used a mouse model of HCC, liver tissues from patients with HCC, and datasets from The Cancer Genome Atlas (TCGA) to elucidate the relationship between mitoribosomal proteins (MRPs) and HCC. In a mouse model, we selectively disrupted expression of the mitochondrial ribosomal protein CR6-interacting factor 1 (CRIF1) in hepatocytes to determine the impact of hepatocyte-specific impairment of mitoribosomal function on liver cancer progression. The metabolism and immunophenotype of liver cancer was assessed by glucose flux assays and flow cytometry, respectively.
resultsSingle-cell RNA-seq analysis of tumor tissue and TCGA HCC transcriptome analysis identified mitochondrial defects associated with high-MRP expression and poor survival outcomes. In the mouse model, hepatocyte-specific disruption of the mitochondrial ribosomal protein CRIF1 revealed the impact of mitoribosomal dysfunction on liver cancer progression.
conclusionsHepatic mitoribosomal defects promote glucose partitioning toward glycolytic flux and lactate synthesis, leading to T cell exhaustion and cancer progression. Overall, the results suggest a distinct role for mitoribosomes in regulating the immunometabolic microenvironment during HCC progression.
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