Evidence map›Paper›PMID 29215776›Full record

ArticleMolecular oncology2018

TGF-β transactivates EGFR and facilitates breast cancer migration and invasion through canonical Smad3 and ERK/Sp1 signaling pathways.

Yuanyuan Zhao, Jing Ma, Yanling Fan, Zhiyong Wang, Ran Tian, Wei Ji, Fei Zhang, Ruifang Niu

Open access · goldAbstract read
In one paragraph

Article in Molecular oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers.

0numbers the graph read from it
0cells of the map it votes in
109citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

109 citing papers in PubMed, 177 citations in OpenAlex.

  1. Association ofBioscience reports · 2019
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  10. Bioinformatic Approach to Identify Positive PrognosticInternational journal of molecular sciences · 2025
    Article
  11. The critical role of LRG1 in pathological fibrosis.Journal of molecular medicine (Berlin, Germany) · 2025
    Review
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  18. Active Substances from the Micro-Immunotherapy Medicine 2LC1International journal of molecular sciences · 2025
    Article
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  20. Review

49 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

8 authors at 1 institution in 1 country.

Yuanyuan ZhaoPublic Laboratory, National Clinical Research Center for Cancer, Tianjin Medical University Cancer Institute and Hospital, China.
Jing MaPublic Laboratory, National Clinical Research Center for Cancer, Tianjin Medical University Cancer Institute and Hospital, China.
Yanling FanPublic Laboratory, National Clinical Research Center for Cancer, Tianjin Medical University Cancer Institute and Hospital, China.
Zhiyong WangPublic Laboratory, National Clinical Research Center for Cancer, Tianjin Medical University Cancer Institute and Hospital, China.
Ran TianPublic Laboratory, National Clinical Research Center for Cancer, Tianjin Medical University Cancer Institute and Hospital, China.
Wei JiPublic Laboratory, National Clinical Research Center for Cancer, Tianjin Medical University Cancer Institute and Hospital, China.
Fei ZhangPublic Laboratory, National Clinical Research Center for Cancer, Tianjin Medical University Cancer Institute and Hospital, China.
Ruifang NiuPublic Laboratory, National Clinical Research Center for Cancer, Tianjin Medical University Cancer Institute and Hospital, China.
Tianjin Medical University Cancer Institute and Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transforming growth factor-beta (TGF-β) functions as a potent proliferation inhibitor and apoptosis inducer in the early stages of breast cancer, yet promotes cancer aggressiveness in the advanced stages. The dual effect of TGF-β on cancer development is known as TGF-β paradox, and the remarkable functional conversion of TGF-β is a pivotal and controversial phenomenon that has been widely investigated for decades. This phenomenon may be attributed to the cross talk between TGF-β signaling and other pathways, including EGF receptor (EGFR) signaling during cancer progression. However, the underlying mechanism by which TGF-β shifts its role from a tumor suppressor to a cancer promoter remains elusive. In this study, TGF-β is positively correlated with EGFR expression in breast cancer tissues, and a functional linkage is observed between TGF-β signaling and EGFR transactivation in breast cancer cell lines. TGF-β promotes the migration and invasion abilities of breast cancer cells, along with the increase in EGFR expression. EGFR is also essential for TGF-β-induced enhancement of these abilities of breast cancer cells. Canonical Smad3 signaling and ERK/Sp1 signaling pathways mediate TGF-β-induced EGFR upregulation. Hence, our study provided insights into a novel mechanism by which TGF-β supports breast cancer progression.

Indexed as

Breast NeoplasmsCell Line, TumorCell MovementErbB ReceptorsFemaleGene Knockdown TechniquesHumansMAP Kinase Signaling SystemNeoplasm InvasivenessSmad3 ProteinSp1 Transcription FactorTransforming Growth Factor betaEGFR protein, humanErbB ReceptorsSmad3 ProteinSMAD3 protein, humanSP1 protein, humanSp1 Transcription FactorTransforming Growth Factor betabreast cancerEGF receptorinvasionSmad3Sp1transforming growth factor-β

Identifiers

PMID29215776
PMCPMC5830653
OpenAlexW2774736917

What OpenQuestion holds

Textmetadata
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.