Evidence map›Paper›PMID 30483746›Full record

ArticleMolecular medicine reports2019

Human adipose‑derived mesenchymal stem cells promote breast cancer MCF7 cell epithelial‑mesenchymal transition by cross interacting with the TGF‑β/Smad and PI3K/AKT signaling pathways.

Simeng Wu, Yajun Wang, Zhe Yuan, Siliang Wang, Hongmei Du, Xue Liu, Qiushi Wang, Xike Zhu

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
1.7field-weighted citation impact, top 12% 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

37 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
  2. Integrative Approaches to Treating Cellular Senescence in Kidney Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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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

8 authors at 1 institution in 1 country.

Simeng WuResearch Center, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China.
Yajun WangResearch Center, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China.
Zhe YuanCord Blood Bank, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China.
Siliang WangDepartment of Medical Oncology, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China.
Hongmei DuDepartment of Medical Oncology, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China.
Xue LiuResearch Center, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China.
Qiushi WangDepartment of Blood Transfusion, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China.
Xike ZhuResearch Center, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China.
China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The influence and underlying mechanisms of human adipose‑derived stem cells (Hu‑ADSCs) on breast cancer cells in the tumor microenvironment remain unclear. Understanding the association between Hu‑ADSCs and cancer cells may provide targets for breast cancer treatment and reference for the clinical application of stem cells. Therefore, a Hu‑ADSC and breast cancer MCF7 cell coculture system was established to investigate the paracrine effects of Hu‑ADSCs on MCF7 cell migration and invasion, in addition to the potential mechanism of action by reverse transcription‑quantitative polymerase chain reaction and western blotting. Hu‑ADSCs enhanced MCF7 cell migration and invasion by decreasing the expression of epithelial marker E‑cadherin, and increasing the expression of interstitial marker N‑cadherin and epithelial‑mesenchymal transition (EMT) transcription factors in vitro. The EMT effect of cocultured MCF7 cells was inhibited with the addition of anti‑transforming growth factor (TGF)‑β1 or phosphoinositide 3‑kinase (PI3K) inhibitor LY294002, accompanied by a significant decrease in phosphorylated (p)‑mothers against decapentaplegic homolog (Smad) and p‑protein kinase B (AKT) expression. The data suggested that the paracrine effect of Hu‑ADSCs in the tumor microenvironment promoted the EMT of MCF7 cells by cross interacting with the TGF‑β/Smad and PI3K/AKT pathways.

Indexed as

Adipose TissueAdultBiomarkers, TumorBreast NeoplasmsCadherinsCell Line, TumorCell MovementCoculture TechniquesEpithelial-Mesenchymal TransitionFemaleHumansMCF-7 CellsMesenchymal Stem CellsNeoplasm InvasivenessPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktBiomarkers, TumorCadherinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSmad ProteinsTransforming Growth Factor betaco-culturecross-interactingHu-ADSCsMCF7 cellsparacrine

Identifiers

PMID30483746
PMCPMC6297785
OpenAlexW2900741281

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.