Evidence map›Paper›PMID 39587064›Full record

ArticleCell death & disease2024

Inhibition of lung tumorigenesis by transient reprogramming in cancer cells.

Pablo Pedrosa, Zhenguang Zhang, Victor Nuñez-Quintela, David Macias, Jianfeng Ge, Mary Denholm, Anna Dyas, Valentin Estevez-Souto, Patricia Lado-Fernandez, Patricia Gonzalez and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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.

Pablo Pedrosa *Cell Senescence, Cancer and Aging Laboratory, Health Research Institute of Santiago de Compostela (IDIS), Santiago de Compostela, Spain.
Zhenguang Zhang *Early Cancer Institute, Department of Oncology, University of Cambridge, Cambridge, UK.ORCID 0000-0002-8317-3163
Victor Nuñez-QuintelaEarly Cancer Institute, Department of Oncology, University of Cambridge, Cambridge, UK.
David MaciasEarly Cancer Institute, Department of Oncology, University of Cambridge, Cambridge, UK.ORCID 0000-0002-8676-1964
Jianfeng GeEarly Cancer Institute, Department of Oncology, University of Cambridge, Cambridge, UK.
Mary DenholmEarly Cancer Institute, Department of Oncology, University of Cambridge, Cambridge, UK.ORCID 0000-0001-5875-4487
Anna DyasEarly Cancer Institute, Department of Oncology, University of Cambridge, Cambridge, UK.
Valentin Estevez-SoutoCell Senescence, Cancer and Aging Laboratory, Health Research Institute of Santiago de Compostela (IDIS), Santiago de Compostela, Spain.ORCID 0000-0003-4724-358X
Patricia Lado-FernandezCell Senescence, Cancer and Aging Laboratory, Health Research Institute of Santiago de Compostela (IDIS), Santiago de Compostela, Spain.ORCID 0000-0002-3572-0257
Patricia GonzalezHistopathology Unit, Spanish National Cancer Research Centre (CNIO), Madrid, Spain.
Maria GomezHistopathology Unit, Spanish National Cancer Research Centre (CNIO), Madrid, Spain.
Jose Ezequiel MartinCMDL, Department of Oncology, SMCL, Department of Medical Genetics, University of Cambridge, Cambridge, UK.
Sabela Da Silva-AlvarezCell Senescence, Cancer and Aging Laboratory, Health Research Institute of Santiago de Compostela (IDIS), Santiago de Compostela, Spain.
Manuel ColladoCell Senescence, Cancer and Aging Laboratory, Health Research Institute of Santiago de Compostela (IDIS), Santiago de Compostela, Spain. manuel.collado.rodriguez@sergas.es.ORCID 0000-0002-0330-0880
Daniel Muñoz-EspínEarly Cancer Institute, Department of Oncology, University of Cambridge, Cambridge, UK. dm742@cam.ac.uk.ORCID 0000-0002-0550-9514

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oncogenic transformation and Oct4, Sox2, Klf4 and c-Myc (OSKM)-mediated induction of pluripotency are two independent and incompatible cellular fates. While continuous expression of OSKM can convert normal somatic cells into teratogenic pluripotent cells, it remains speculative what is the impact of transient OSKM expression in cancer cells. Here, we find that OSKM expression limits the growth of transformed lung cells by inducing apoptosis and senescence. We identify Oct4 and Klf4 as the main individual reprogramming factors responsible for this effect. Mechanistically, the induction of cell cycle inhibitor p21 downstream of the reprogramming factors acts as mediator of cell death and senescence. Using a variety of in vivo systems, including allografts, orthotopic transplantation and KRAS-driven lung cancer mouse models, we demonstrate that transient reprogramming by OSKM expression in cancer cells impairs tumor growth and reduces tumor burden. Altogether, our results show that the induction of transient reprogramming in cancer cells is antitumorigenic opening novel potential therapeutic avenues in oncology.

Indexed as

Cellular ReprogrammingKruppel-Like Factor 4Lung NeoplasmsOctamer Transcription Factor-3AnimalsApoptosisCarcinogenesisCell Line, TumorCell Transformation, NeoplasticCellular SenescenceCyclin-Dependent Kinase Inhibitor p21HumansKruppel-Like Transcription FactorsMiceProto-Oncogene Proteins c-mycSOXB1 Transcription FactorsCyclin-Dependent Kinase Inhibitor p21KLF4 protein, humanKlf4 protein, mouseKruppel-Like Factor 4Kruppel-Like Transcription FactorsOctamer Transcription Factor-3POU5F1 protein, humanProto-Oncogene Proteins c-mycSOXB1 Transcription Factors

Identifiers

PMID39587064
PMCPMC11589828

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.