ArticleCell death and differentiation2018
Carnitine palmitoyltransferase 1C regulates cancer cell senescence through mitochondria-associated metabolic reprograming.
Article in Cell death and differentiation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.
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The trial behind it
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Who cites it
44 citing papers in PubMed, 1 synthesis or guideline pooled it, 92 citations in OpenAlex.
- A novel miR-1291-ERRα-CPT1C axis modulates tumor cell proliferation, metabolism and tumorigenesis.Theranostics · 2020Pooled it
- Trial
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- Combining machine learning and multi-omics analysis to explore the role of CPT1C in colorectal tumor cancer transformation.Scientific reports · 2026Article
- Beyond Bioenergetics: Emerging Roles of Mitochondrial Fatty Acid Oxidation in Stress Response and Aging.Cells · 2025Review
- Causal associations between circulating metabolites and risk of neuroblastoma: a bidirectional Mendelian randomization study.Discover oncology · 2025Article
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- Identification and Validation of Biomarkers in Chronic Rhinosinusitis With Nasal Polyps and Study of Their Associated Mechanisms.World journal of otorhinolaryngology - head and neck surgery · 2025Article
- Mitochondrial Reverse Electron Transport: Mechanisms, Pathophysiological Roles, and Therapeutic Potential.Biology · 2025Review
- Application of Metabolic Biomarkers in Breast Cancer: A Literature Review.Annals of laboratory medicine · 2025Review
- Linking microRNA to metabolic reprogramming and gut microbiota in the pathogenesis of colorectal cancer (Review).International journal of molecular medicine · 2025Review
- Review
- Genetically predicted gut bacteria, circulating bacteria-associated metabolites and pancreatic ductal adenocarcinoma: a Mendelian randomisation study.Scientific reports · 2024Article
- Review
- METTL3 promotes cellular senescence of colorectal cancer via modulation of CDKN2B transcription and mRNA stability.Oncogene · 2024Article
- The role of serum acylcarnitine profiling for the detection of multiple solid tumors in humans.Heliyon · 2024Article
- Unraveling the intricate relationship between lipid metabolism and oncogenic signaling pathways.Frontiers in cell and developmental biology · 2024Review
- PRRG4 regulates mitochondrial function and promotes migratory behaviors of breast cancer cells through the Src-STAT3-POLG axis.Cancer cell international · 2023Article
- Precision-Cut Liver Slices as anbioRxiv : the preprint server for biology · 2023Article
- Serum Metabolite Biomarkers for Pancreatic Tumors: Neuroendocrine and Pancreatic Ductal Adenocarcinomas-A Preliminary Study.Cancers · 2023Article
Corrections and comments
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Authors and funding
16 authors at 6 institutions in 2 countries.
Funding
Abstract
Cellular senescence is a fundamental biological process that has profound implications in cancer development and therapeutics, but the underlying mechanisms remain elusive. Here we show that carnitine palmitoyltransferase 1C (CPT1C), an enzyme that catalyzes carnitinylation of fatty acids for transport into mitochondria for β-oxidation, plays a major role in the regulation of cancer cell senescence through mitochondria-associated metabolic reprograming. Metabolomics analysis suggested alterations in mitochondria activity, as revealed by the marked decrease in acylcarnitines in senescent human pancreatic carcinoma PANC-1 cells, indicating low CPT1C activity. Direct analyses of mRNA and protein show that CPT1C is significantly reduced in senescent cells. Furthermore, abnormal mitochondrial function was observed in senescent PANC-1 cells, leading to lower cell survival under metabolic stress and suppressed tumorigenesis in a mouse xenograft model. Knock-down of CPT1C in PANC-1 cells induced mitochondrial dysfunction, caused senescence-like growth suppression and cellular senescence, suppressed cell survival under metabolic stress, and inhibited tumorigenesis in vivo. Further, CPT1C knock-down suppressed xenograft tumor growth in situ. Silencing of CPT1C in five other tumor cell lines also caused cellular senescence. On the contrary, gain-of-function of CPT1C reversed PANC-1 cell senescence and enhanced mitochondrial function. This study identifies CPT1C as a novel biomarker and key regulator of cancer cell senescence through mitochondria-associated metabolic reprograming, and suggests that inhibition of CPT1C may represent a new therapeutic strategy for cancer treatment through induction of tumor senescence.
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Registered trials
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.