Evidence map›Paper›PMID 40319202›Full record

ArticleBritish journal of cancer2025

SMAD2 linker phosphorylation impacts overall survival, proliferation, TGFβ1-dependent gene expression and pluripotency-related proteins in NSCLC.

Dörte Nitschkowski, Tim Vierbuchen, Holger Heine, Jochen Behrends, Norbert Reiling, Martin Reck, Klaus F Rabe, Christian Kugler, Ole Ammerpohl, Daniel Drömann and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in British journal of cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

16 authors.

Dörte NitschkowskiHistology, Research Center Borstel - Leibniz Lung Center, Borstel, Germany. dnitschkowski@fz-borstel.de.ORCID http://orcid.org/0000-0002-5347-6403
Tim VierbuchenDivision of Innate Immunity, Research Center Borstel - Leibniz Lung Center, Borstel, Germany.
Holger HeineAirway Research Center North (ARCN), Member of the German Center for Lung Research (DZL), Borstel, Lübeck and Großhansdorf, Germany.ORCID http://orcid.org/0000-0001-8128-5068
Jochen BehrendsCore Facility Fluorescence Cytometry, Research Center Borstel - Leibniz Lung Center, Borstel, Germany.
Norbert ReilingMicrobial Interface Biology, Research Center Borstel - Leibniz Lung Center, Borstel, Germany.
Martin ReckAirway Research Center North (ARCN), Member of the German Center for Lung Research (DZL), Borstel, Lübeck and Großhansdorf, Germany.
Klaus F RabeAirway Research Center North (ARCN), Member of the German Center for Lung Research (DZL), Borstel, Lübeck and Großhansdorf, Germany.
Christian KuglerAirway Research Center North (ARCN), Member of the German Center for Lung Research (DZL), Borstel, Lübeck and Großhansdorf, Germany.
Ole AmmerpohlAirway Research Center North (ARCN), Member of the German Center for Lung Research (DZL), Borstel, Lübeck and Großhansdorf, Germany.
Daniel DrömannAirway Research Center North (ARCN), Member of the German Center for Lung Research (DZL), Borstel, Lübeck and Großhansdorf, Germany.
Thomas MuleyTranslational Research Unit, Thoraxklinik at Heidelberg University Hospital, Heidelberg, Germany.ORCID http://orcid.org/0000-0002-8141-0604
Mark KriegsmannTranslational Lung Research Center Heidelberg (TLRC-H), Member of the German Center for Lung Research (DZL), Heidelberg, Germany.
Georgious T StathopoulosHelmholtz Center Munich, Molecular Carcinogenesis, Munich, Germany.
Kristina A M ArendtHelmholtz Center Munich, Molecular Carcinogenesis, Munich, Germany.
Torsten Goldmann *Histology, Research Center Borstel - Leibniz Lung Center, Borstel, Germany.
Sebastian Marwitz *Histology, Research Center Borstel - Leibniz Lung Center, Borstel, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundWe investigated the impact of SMAD2 linker phosphorylation (pSMAD2L) on overall and disease-free survival, signal transduction, as well as cancer-related processes in non-small cell lung cancer (NSCLC).

methodsWe generated A549 cells constitutively lacking pSMAD2L (A549L

resultsIn NSCLC cell lines and benign T cells, pSMAD2L was expressed in a mitosis-dependent manner. Loss of pSMAD2L (A549L

conclusionspSMAD2L antagonises anti-proliferative canonical TGFβ-signalling in NSCLC and redirects TGFβ1-dependent gene expression, whereas loss of pSMAD2L enhances SMAD2

Indexed as

Carcinoma, Non-Small-Cell LungLung NeoplasmsSmad2 ProteinTransforming Growth Factor beta1A549 CellsCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansMalePhosphorylationSignal TransductionSmad2 ProteinSMAD2 protein, humanTGFB1 protein, humanTransforming Growth Factor beta1

Identifiers

PMID40319202
PMCPMC12238225

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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.