Evidence map›Paper›PMID 36693836›Full record

ReviewCell death & disease2023

To be or not to be a fat burner, that is the question for cpt1c in cancer cells.

Rut Fadó, Sebastian Zagmutt, Laura Herrero, Helena Muley, Rosalía Rodríguez-Rodríguez, Huichang Bi, Dolors Serra, Núria Casals

Open access · goldAbstract readReview
In one paragraph

Review in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
5.3field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Sirtuins, redox, and metabolic pathways in the brain of female PCOS mice.Journal of assisted reproduction and genetics · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 2 countries.

Rut FadóBasic Sciences Department, Faculty of Medicine and Health Sciences, Universitat Internacional de Catalunya, E-08195, Sant Cugat del Vallès, Spain.
Sebastian ZagmuttBasic Sciences Department, Faculty of Medicine and Health Sciences, Universitat Internacional de Catalunya, E-08195, Sant Cugat del Vallès, Spain.
Laura HerreroDepartment of Biochemistry and Physiology, School of Pharmacy and Food Sciences, Universitat de Barcelona, E-08028, Barcelona, Spain.ORCID 0000-0003-4244-4673
Helena MuleyBasic Sciences Department, Faculty of Medicine and Health Sciences, Universitat Internacional de Catalunya, E-08195, Sant Cugat del Vallès, Spain.
Rosalía Rodríguez-RodríguezBasic Sciences Department, Faculty of Medicine and Health Sciences, Universitat Internacional de Catalunya, E-08195, Sant Cugat del Vallès, Spain.
Huichang BiSchool of Pharmaceutical Sciences, Southern Medical University, Guangzhou, 510515, China. bihchang@smu.edu.cn.
Dolors SerraDepartment of Biochemistry and Physiology, School of Pharmacy and Food Sciences, Universitat de Barcelona, E-08028, Barcelona, Spain.ORCID 0000-0002-4936-4206
Núria CasalsBasic Sciences Department, Faculty of Medicine and Health Sciences, Universitat Internacional de Catalunya, E-08195, Sant Cugat del Vallès, Spain. ncasals@uic.es.ORCID 0000-0002-6719-4300
Instituto de Salud Carlos III · ESUniversitat Internacional de Catalunya · ESSouthern Medical University · CNUniversitat Autònoma de Barcelona · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There is an urgent need to identify reliable genetic biomarkers for accurate diagnosis, prognosis, and treatment of different tumor types. Described as a prognostic marker for many tumors is the neuronal protein carnitine palmitoyltransferase 1 C (CPT1C). Several studies report that CPT1C is involved in cancer cell adaptation to nutrient depletion and hypoxia. However, the molecular role played by CPT1C in cancer cells is controversial. Most published studies assume that, like canonical CPT1 isoforms, CPT1C is a mediator of fatty acid transport to mitochondria for beta-oxidation, despite the fact that CPT1C has inefficient catalytic activity and is located in the endoplasmic reticulum. In this review, we collate existing evidence on CPT1C in neurons, showing that CPT1C is a sensor of nutrients that interacts with and regulates other proteins involved in lipid metabolism and transport, lysosome motility, and the secretory pathway. We argue, therefore, that CPT1C expression in cancer cells is not a direct regulator of fat burn, but rather is a regulator of lipid metabolic reprograming and cell adaptation to environmental stressors. We also review the clinical relevance of CPT1C as a prognostic indicator and its contribution to tumor growth, cancer invasiveness, and cell senescence. This new and integrated vision of CPT1C function can help better understand the metabolic plasticity of cancer cells and improve the design of therapeutic strategies.

Indexed as

Carnitine O-PalmitoyltransferaseNeoplasmsHumansHypoxiaNeuronsOxidation-ReductionCarnitine O-PalmitoyltransferaseCPT1B protein, human

Identifiers

PMID36693836
PMCPMC9873675
OpenAlexW4317821593

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.