Evidence map›Paper›PMID 25064833›Full record

ArticleNature chemical biology2014

The solute carrier SLC35F2 enables YM155-mediated DNA damage toxicity.

Georg E Winter, Branka Radic, Cristina Mayor-Ruiz, Vincent A Blomen, Claudia Trefzer, Richard K Kandasamy, Kilian V M Huber, Manuela Gridling, Doris Chen, Thorsten Klampfl and 5 more

Abstract read
In one paragraph

Article in Nature chemical biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed
10.7field-weighted citation impact, top 1% 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

85 citing papers in PubMed, 182 citations in OpenAlex.

  1. Review
  2. The oncogene SLC35F2 is a high-specificity transporter for the micronutrients queuine and queuosine.Proceedings of the National Academy of Sciences of the United States of America · 2025
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25 more citing papers are in PubMed but not listed here.

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

15 authors at 3 institutions in 3 countries.

Georg E WinterCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Lazarettgasse 14 1090 Vienna, Austria.
Branka Radic *CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Lazarettgasse 14 1090 Vienna, Austria.
Cristina Mayor-Ruiz *CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Lazarettgasse 14 1090 Vienna, Austria.
Vincent A BlomenDivision of Biochemistry, The Netherlands Cancer Institute, 1066 CX Amsterdam, The Netherlands.
Claudia TrefzerCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Lazarettgasse 14 1090 Vienna, Austria.
Richard K KandasamyCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Lazarettgasse 14 1090 Vienna, Austria.
Kilian V M HuberCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Lazarettgasse 14 1090 Vienna, Austria.
Manuela GridlingCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Lazarettgasse 14 1090 Vienna, Austria.
Doris ChenCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Lazarettgasse 14 1090 Vienna, Austria.
Thorsten KlampflCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Lazarettgasse 14 1090 Vienna, Austria.
Robert KralovicsCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Lazarettgasse 14 1090 Vienna, Austria.
Stefan KubicekCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Lazarettgasse 14 1090 Vienna, Austria.
Oscar Fernandez-CapetilloGenomic Instability Group, Spanish National Cancer Research Centre (CNIO), Madrid, Spain.
Thijn R BrummelkampCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Lazarettgasse 14 1090 Vienna, Austria.
Giulio Superti-FurgaCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Lazarettgasse 14 1090 Vienna, Austria.
Austrian Academy of Sciences · ATSpanish National Cancer Research Centre · ESThe Netherlands Cancer Institute · NL

Funding

European Research Council 617840Worldwide Cancer Research 12-0229
6 · The paper itself

Abstract

Genotoxic chemotherapy is the most common cancer treatment strategy. However, its untargeted generic DNA-damaging nature and associated systemic cytotoxicity greatly limit its therapeutic applications. Here, we used a haploid genetic screen in human cells to discover an absolute dependency of the clinically evaluated anticancer compound YM155 on solute carrier family member 35 F2 (SLC35F2), an uncharacterized member of the solute carrier protein family that is highly expressed in a variety of human cancers. YM155 generated DNA damage through intercalation, which was contingent on the expression of SLC35F2 and its drug-importing activity. SLC35F2 expression and YM155 sensitivity correlated across a panel of cancer cell lines, and targeted genome editing verified SLC35F2 as the main determinant of YM155-mediated DNA damage toxicity in vitro and in vivo. These findings suggest a new route to targeted DNA damage by exploiting tumor and patient-specific import of YM155.

Indexed as

AnimalsApoptosisCell DivisionCell Line, TumorCell SurvivalCloning, MolecularComet AssayDNA DamageGenome, HumanHaploidyHumansImidazolesImmunohistochemistryIntercalating AgentsMembrane Transport ProteinsMiceImidazolesIntercalating AgentsMembrane Transport ProteinsNaphthoquinonesRNA, NeoplasmsepantroniumSLC35F2 protein, human

Identifiers

PMID25064833
PMCPMC4913867
OpenAlexW2057000572

What OpenQuestion holds

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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.