Evidence map›Paper›PMID 26799588›Full record

ArticleOncotarget2016

Carnitine palmitoyl transferase-1A (CPT1A): a new tumor specific target in human breast cancer.

Sabina Pucci, Maria Josè Zonetti, Tommaso Fisco, Chiara Polidoro, Gianfranco Bocchinfuso, Antonio Palleschi, Giuseppe Novelli, Luigi G Spagnoli, Paola Mazzarelli

Abstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
–field-weighted citation impact
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

59 citing papers in PubMed.

  1. Article
  2. Review
  3. The emerging metabolic role and treatment target of CPT1A in CRC.Frontiers in cell and developmental biology · 2026
    Review
  4. Article
  5. Carnitine Shuttle and Ferroptosis in Cancer.Antioxidants (Basel, Switzerland) · 2025
    Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. ACSL3 regulates breast cancer progressionCancer biology & medicine · 2024
    Article
  13. Article
  14. The Physiological and Pathological Role of Acyl-CoA Oxidation.International journal of molecular sciences · 2023
    Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review
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

9 authors.

Sabina PucciDepartment of Biomedicine and Prevention, Tor Vergata University of Rome, Rome, Italy.
Maria Josè ZonettiDepartment of Biomedicine and Prevention, Tor Vergata University of Rome, Rome, Italy.
Tommaso FiscoDepartment of Biomedicine and Prevention, Tor Vergata University of Rome, Rome, Italy.
Chiara PolidoroDepartment of Biomedicine and Prevention, Tor Vergata University of Rome, Rome, Italy.
Gianfranco BocchinfusoDepartment of Chemical Sciences and Technologies, Tor Vergata University of Rome, Rome, Italy.
Antonio PalleschiDepartment of Chemical Sciences and Technologies, Tor Vergata University of Rome, Rome, Italy.
Giuseppe NovelliDepartment of Biomedicine and Prevention, Tor Vergata University of Rome, Rome, Italy.
Luigi G SpagnoliDepartment of Biomedicine and Prevention, Tor Vergata University of Rome, Rome, Italy.
Paola MazzarelliDepartment of Biomedicine and Prevention, Tor Vergata University of Rome, Rome, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transcriptional mechanisms epigenetically-regulated in tumoral tissues point out new targets for anti-cancer therapies. Carnitine palmitoyl transferase I (CPT1) is the rate-limiting enzyme in the transport of long-chain fatty acids for β-oxidation. Here we identified the tumor specific nuclear CPT1A as a product of the transcript variant 2, that doesn't retain the classical transferase activity and is strongly involved in the epigenetic regulation of cancer pro-survival, cell death escaping and tumor invasion pathways. The knockdown of CPT1A variant 2 by small interfering RNAs (siRNAs), was sufficient to induce apoptosis in MCF-7, SK-BR3 and MDA-MB-231 breast cancer cells. The cell death triggered by CPT1A silencing correlated with reduction of HDAC activity and histone hyperacetylation. Docking experiments and molecular dynamics simulations confirmed an high binding affinity of the variant 2 for HDAC1. The CPT1A silenced cells showed an up-regulated transcription of pro-apoptotic genes (BAD, CASP9, COL18A1) and down-modulation of invasion and metastasis related-genes (TIMP-1, PDGF-A, SERPINB2). These findings provide evidence of the CPT1 variant 2 involvement in breast cancer survival, cell death escape and invasion. Thus, we propose nuclear CPT1A as a striking tumor specific target for anticancer therapeutics, more selective and effective as compared with the well-known HDAC inhibitors.

Indexed as

Gene Expression Regulation, NeoplasticApoptosisBiomarkers, TumorBreast NeoplasmsCarnitine O-PalmitoyltransferaseCell ProliferationEpigenesis, GeneticFemaleHistone Deacetylase 1HumansMolecular Dynamics SimulationOxidation-ReductionTumor Cells, CulturedBiomarkers, TumorCarnitine O-PalmitoyltransferaseCPT1A protein, humanHDAC1 protein, humanHistone Deacetylase 1breast cancercarnitine palmitoyl transferase-1AHDAC inhibitortumor metabolismtumor specific target

Identifiers

PMID26799588
PMCPMC4991433

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Registered trials

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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.