ArticleJournal of experimental & clinical cancer research : CR2024
UBASH3B-mediated MRPL12 Y60 dephosphorylation inhibits LUAD development by driving mitochondrial metabolism reprogramming.
Article in Journal of experimental & clinical cancer research : CR, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- The Proteome of Bone Marrow Multipotent Mesenchymal Stromal Cells Undergoes Significant Alterations in Acute Leukemia Patients at the Onset and During Treatment.International journal of molecular sciences · 2026Article
- Dual regulation of metabolic reprogramming and protein competitive modifications: the core role and mechanism of MRPL36 in glioblastoma malignant progression.Journal of experimental & clinical cancer research : CR · 2026Article
- Optimized deep intelligent parameter efficient fine-tuning protein language model system for predicting dephosphorylation site.Journal of molecular modeling · 2026Article
- Comprehensive analysis of liquid-liquid phase separation-related genes in osteosarcoma: implications for prognosis, immune infiltration and drug sensitivity.Translational cancer research · 2026Article
- The role of mitochondrial energy metabolism in drug resistance and prognosis of lung adenocarcinoma: a multi-omics and machine learning strategy for predictive and personalized therapy.Frontiers in medicine · 2026Article
- Co-targeting MRPS7-23 synergistically enhances cisplatin efficacy to suppress nasopharyngeal carcinoma growth and metastasis.International journal of biological sciences · 2026Article
- Spatiotemporal control of mitoribosome-mediated metabolic reprogramming in cancer: implications for heterogeneity and therapeutic targeting.Frontiers in cell and developmental biology · 2026Review
- Mitochondrial ribosomal protein L12 mediates metabolic reorganization in clear cell renal cell carcinoma by regulating mitochondrial biosynthesis.Cell communication and signaling : CCS · 2025Article
- Investigating the role of UBASH3B in cancer: structural relevance, physiological functions, and therapeutic possibilities.Journal of experimental & clinical cancer research : CR · 2025Review
- MRPL12 K163 acetylation inhibits ccRCC via driving mitochondrial metabolic reprogramming.Cell death & disease · 2025Article
- MRPL13 enhances mitochondrial function and promotes tumor progression in ovarian cancer by inhibiting mPTP opening via SLC25A6.Cell death & disease · 2025Article
- The pathogenesis and therapeutic implications of metabolic reprogramming in renal cell carcinoma.Cell death discovery · 2025Review
- Mitochondrial Ribosomal Proteins and Cancer.Medicina (Kaunas, Lithuania) · 2025Review
- Mitochondrial ribosomal proteins: potential targets for cancer prognosis and therapy.Frontiers in oncology · 2025Review
- Integration of multi-omics and single-cell transcriptome reveals mitochondrial outer membrane protein-2 (MTX-2) as a prognostic biomarker and characterizes ubiquinone metabolism in lung adenocarcinoma.Journal of Cancer · 2025Article
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13 authors.
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Abstract
backgroundMetabolic reprogramming plays a pivotal role in tumorigenesis and development of lung adenocarcinoma (LUAD). However, the precise mechanisms and potential targets for metabolic reprogramming in LUAD remain elusive. Our prior investigations revealed that the mitochondrial ribosomal protein MRPL12, identified as a novel mitochondrial transcriptional regulatory gene, exerts a critical influence on mitochondrial metabolism. Despite this, the role and regulatory mechanisms underlying MRPL12's transcriptional activity in cancers remain unexplored.
methodsHuman LUAD tissues, Tp53
resultsMRPL12 was upregulated in human LUAD tissues, Tp53
conclusionThis study establishes MRPL12 as a novel oncogene in LUAD, contributing to LUAD pathogenesis by orchestrating mitochondrial metabolism reprogramming towards oxidative phosphorylation (OXPHOS). Furthermore, it confirms Y60 as a specific phosphorylation modification site regulating MRPL12's oncogenic functions, offering insights for the development of LUAD-specific targeted drugs and clinical interventions.
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