Evidence map›Paper›PMID 36450103›Full record

ArticleJournal of proteome research2023

Multiomics of Colorectal Cancer Organoids Reveals Putative Mediators of Cancer Progression Resulting from SMAD4 Inactivation.

Jelmer J Dijkstra, Hannah K Neikes, Somayeh Rezaeifard, Xuhui Ma, Emile E Voest, Daniele V F Tauriello, Michiel Vermeulen

Open access · hybridAbstract read
In one paragraph

Article in Journal of proteome research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

14 citing papers in PubMed, 17 citations in OpenAlex.

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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

7 authors at 2 institutions in 2 countries.

Jelmer J DijkstraDepartment of Molecular Biology, Faculty of Science, Radboud Institute for Molecular Life Sciences (RIMLS), Oncode Institute, Radboud University Nijmegen, Geert Grooteplein 26-28, 6525 GA Nijmegen, The Netherlands.
Hannah K NeikesDepartment of Molecular Biology, Faculty of Science, Radboud Institute for Molecular Life Sciences (RIMLS), Oncode Institute, Radboud University Nijmegen, Geert Grooteplein 26-28, 6525 GA Nijmegen, The Netherlands.
Somayeh RezaeifardDepartment of Cell Biology, Radboud University Medical Center/Radboud Institute for Molecular Life Sciences (RIMLS), Radboud University Nijmegen, Geert Grooteplein 26-28, 6525 GA Nijmegen, The Netherlands.
Xuhui MaDepartment of Molecular Oncology and Immunology, Oncode Institute, The Netherlands Cancer Institute, Antoni van Leeuwenhoek Hospital, 1066 CX Amsterdam, The Netherlands.
Emile E VoestDepartment of Molecular Oncology and Immunology, Oncode Institute, The Netherlands Cancer Institute, Antoni van Leeuwenhoek Hospital, 1066 CX Amsterdam, The Netherlands.
Daniele V F TaurielloDepartment of Cell Biology, Radboud University Medical Center/Radboud Institute for Molecular Life Sciences (RIMLS), Radboud University Nijmegen, Geert Grooteplein 26-28, 6525 GA Nijmegen, The Netherlands.
Michiel VermeulenDepartment of Molecular Biology, Faculty of Science, Radboud Institute for Molecular Life Sciences (RIMLS), Oncode Institute, Radboud University Nijmegen, Geert Grooteplein 26-28, 6525 GA Nijmegen, The Netherlands.ORCID 0000-0003-0836-6894
Radboud University Nijmegen · NLThe Netherlands Cancer Institute · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The development of metastasis severely reduces the life expectancy of patients with colorectal cancer (CRC). Although loss of SMAD4 is a key event in CRC progression, the resulting changes in biological processes in advanced disease and metastasis are not fully understood. Here, we applied a multiomics approach to a CRC organoid model that faithfully reflects the metastasis-supporting effects of SMAD4 inactivation. We show that loss of SMAD4 results in decreased differentiation and activation of pro-migratory and cell proliferation processes, which is accompanied by the disruption of several key oncogenic pathways, including the TGFβ, WNT, and VEGF pathways. In addition, SMAD4 inactivation leads to increased secretion of proteins that are known to be involved in a variety of pro-metastatic processes. Finally, we show that one of the factors that is specifically secreted by

Indexed as

Colorectal NeoplasmsMultiomicsCell Line, TumorCell ProliferationHumansSmad4 ProteinTransforming Growth Factor betaSmad4 ProteinSMAD4 protein, humanTransforming Growth Factor betacancer progressioncolorectal cancermultiomicssecretomicsSMAD4

Identifiers

PMID36450103
PMCPMC9830641
OpenAlexW4310570044

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.