Evidence map›Paper›PMID 35214160›Full record

ArticlePharmaceutics2022

Anticancer Activity of the Choline Kinase Inhibitor PL48 Is Due to Selective Disruption of Choline Metabolism and Transport Systems in Cancer Cell Lines.

Pablo García-Molina, Alberto Sola-Leyva, Pilar M Luque-Navarro, Alejandro Laso, Pablo Ríos-Marco, Antonio Ríos, Daniela Lanari, Archimede Torretta, Emilio Parisini, Luisa C López-Cara and 2 more

Open access · goldAbstract read
In one paragraph

Article in Pharmaceutics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.8field-weighted citation impact, top 32% 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

5 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Observational
  5. 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

12 authors at 3 institutions in 3 countries.

Pablo García-MolinaDepartment of Biochemistry and Molecular Biology I, University of Granada, 18071 Granada, Spain.
Alberto Sola-LeyvaDepartment of Biochemistry and Molecular Biology I, University of Granada, 18071 Granada, Spain.ORCID 0000-0003-1388-1532
Pilar M Luque-NavarroDepartment of Pharmaceutical and Organic Chemistry, University of Granada, 18071 Granada, Spain.
Alejandro LasoDepartment of Biochemistry and Molecular Biology I, University of Granada, 18071 Granada, Spain.
Pablo Ríos-MarcoDepartment of Biochemistry and Molecular Biology I, University of Granada, 18071 Granada, Spain.
Antonio RíosDepartment of Cell Biology, University of Granada, 18071 Granada, Spain.
Daniela LanariDepartment of Pharmaceutical Sciences, University of Perugia, 06123 Perugia, Italy.
Archimede TorrettaCenter for Nano Science and Technology @Polimi, Istituto Italiano di Tecnologia, Via Pascoli 70/3, 20133 Milano, Italy.
Emilio ParisiniCenter for Nano Science and Technology @Polimi, Istituto Italiano di Tecnologia, Via Pascoli 70/3, 20133 Milano, Italy.ORCID 0000-0002-5529-0039
Luisa C López-CaraDepartment of Pharmaceutical and Organic Chemistry, University of Granada, 18071 Granada, Spain.ORCID 0000-0003-1142-6448
Carmen MarcoDepartment of Biochemistry and Molecular Biology I, University of Granada, 18071 Granada, Spain.
María P Carrasco-JiménezDepartment of Biochemistry and Molecular Biology I, University of Granada, 18071 Granada, Spain.ORCID 0000-0003-1300-5196
Universidad de Granada · ESItalian Institute of Technology · ITUniversity of Perugia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A large number of different types of cancer have been shown to be associated with an abnormal metabolism of phosphatidylcholine (PC), the main component of eukaryotic cell membranes. Indeed, the overexpression of choline kinase α1 (ChoKα1), the enzyme that catalyses the bioconversion of choline to phosphocholine (PCho), has been found to associate with cell proliferation, oncogenic transformation and carcinogenesis. Hence, ChoKα1 has been described as a possible cancer therapeutic target. Moreover, the choline transporter CTL1 has been shown to be highly expressed in several tumour cell lines. In the present work, we evaluate the antiproliferative effect of PL48, a rationally designed inhibitor of ChoKα1, in MCF7 and HepG2 cell lines. In addition, we illustrate that the predominant mechanism of cellular choline uptake in these cells is mediated by the CTL1 choline transporter. A possible correlation between the inhibition of both choline uptake and ChoKα1 activity and cell proliferation in cancer cell lines is also highlighted. We conclude that the efficacy of this inhibitor on cell proliferation in both cell lines is closely correlated with its capability to block choline uptake and ChoKα1 activity, making both proteins potential targets in cancer therapy.

Indexed as

cancercholine kinase inhibitorscholine uptakelipid metabolism

Identifiers

PMID35214160
PMCPMC8876215
OpenAlexW4213378213

What OpenQuestion holds

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LicenceCC BY
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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.