Evidence map›Paper›PMID 30808576›Full record

ReviewEBioMedicine2019

Opposing roles and potential antagonistic mechanism between TGF-β and BMP pathways: Implications for cancer progression.

Junya Ning, Yi Zhao, Yingnan Ye, Jinpu Yu

Open access · goldAbstract readReview
In one paragraph

Review in EBioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

50 citing papers in PubMed, 95 citations in OpenAlex.

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  11. Frontiers in immunology · 2024
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  17. Antagonizing CD105 and androgen receptor to target stromal-epithelial interactions for clinical benefit.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
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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

4 authors at 2 institutions in 1 country.

Junya NingCancer Molecular Diagnostics Core, Tianjin Medical University Cancer Institute & Hospital, National Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin, PR China; Department of Immunology, Tianjin Medical University Cancer Institute & Hospital, National Clinical Research Center of Cancer, Key Laboratory of Cancer Immunology and Biotherapy, Tianjin's Clinical Research Center for Cancer, Tianjin, PR China.
Yi ZhaoKey Laboratory of Intelligent Information Processing, Advanced Computer Research Center, State Key Laboratory of Computer Architecture, Institute of Computing Technology, Chinese Academy of Sciences, Beijing, PR China.
Yingnan YeCancer Molecular Diagnostics Core, Tianjin Medical University Cancer Institute & Hospital, National Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin, PR China.
Jinpu YuCancer Molecular Diagnostics Core, Tianjin Medical University Cancer Institute & Hospital, National Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin, PR China; Department of Immunology, Tianjin Medical University Cancer Institute & Hospital, National Clinical Research Center of Cancer, Key Laboratory of Cancer Immunology and Biotherapy, Tianjin's Clinical Research Center for Cancer, Tianjin, PR China. Electronic address: yujinpu@tjmuch.com.
Tianjin Medical University Cancer Institute and Hospital · CNState Key Laboratory of Computer Architecture

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transforming growth factor β (TGF-β) superfamily participates in tumour proliferation, apoptosis, differentiation, migration, invasion, immune evasion and extracellular matrix remodelling. Genetic deficiency in distinct components of TGF-β and BMP-induced signalling pathways or their excessive activation has been reported to regulate the development and progression of some cancers. As more in-depth studies about this superfamily have been conducted, more evidence suggests that the TGF-β and BMP pathways play an opposing role. The cross-talk of these 2 pathways has been widely studied in kidney disease and bone formation, and the opposing effects have also been observed in some cancers. However, the antagonistic mechanisms are still insufficiently investigated in cancer. In this review, we aim to display more evidences and possible mechanisms accounting for the antagonism between these 2 pathways, which might provide some clues for further study in cancer.

Indexed as

Signal TransductionBone Morphogenetic ProteinsCarrier ProteinsCCCTC-Binding FactorHumansMicroRNAsNeoplasmsSmad ProteinsTransforming Growth Factor betaBone Morphogenetic ProteinsCarrier ProteinsCCCTC-Binding FactorKCP protein, humanMicroRNAsSmad ProteinsTransforming Growth Factor betaTGF-β BMP cancer antagonistic potential mechanism

Identifiers

PMID30808576
PMCPMC6442991
OpenAlexW2916609106

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.