Evidence map›Paper›PMID 30106153›Full record

ArticleMolecular medicine reports2018

Correlation between DEC1/DEC2 and epithelial‑mesenchymal transition in human prostate cancer PC‑3 cells.

Qiang Liu, Yunyan Wu, Hiroko Seino, Toshihiro Haga, Tadashi Yoshizawa, Satoko Morohashi, Hiroshi Kijima

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.6field-weighted citation impact, top 29% 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

12 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
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  4. Review
  5. Article
  6. Co-regulation of circadian clock genes and microRNAs in bone metabolism.Journal of Zhejiang University. Science. B · 2022
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. BHLHE41 suppresses MCF-7 cell invasion via MAPK/JNK pathway.Journal of cellular and molecular medicine · 2020
    Article
  12. 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

7 authors at 1 institution in 1 country.

Qiang LiuDepartment of Pathology and Bioscience, Hirosaki University Graduate School of Medicine, Hirosaki, Aomori 036‑8562, Japan.
Yunyan WuDepartment of Pathology and Bioscience, Hirosaki University Graduate School of Medicine, Hirosaki, Aomori 036‑8562, Japan.
Hiroko SeinoDepartment of Pathology and Bioscience, Hirosaki University Graduate School of Medicine, Hirosaki, Aomori 036‑8562, Japan.
Toshihiro HagaDepartment of Pathology and Bioscience, Hirosaki University Graduate School of Medicine, Hirosaki, Aomori 036‑8562, Japan.
Tadashi YoshizawaDepartment of Pathology and Bioscience, Hirosaki University Graduate School of Medicine, Hirosaki, Aomori 036‑8562, Japan.
Satoko MorohashiDepartment of Pathology and Bioscience, Hirosaki University Graduate School of Medicine, Hirosaki, Aomori 036‑8562, Japan.
Hiroshi KijimaDepartment of Pathology and Bioscience, Hirosaki University Graduate School of Medicine, Hirosaki, Aomori 036‑8562, Japan.
Hirosaki University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Differentiated embryonic chondrocyte (DEC) genes have been reported to be involved in the regulation of mammalian circadian rhythms, differentiation, apoptosis, the response to hypoxia and epithelial‑mesenchymal transition (EMT). Activation of transforming growth factor (TGF)‑β signaling is known to promote EMT for the development of metastatic castration‑resistant prostate cancer (PCa). However, the role of DEC genes in the TGF‑β‑induced EMT of PCa remains unclear. In the present study it was demonstrated that TGF‑β increased the transcriptional/translational levels of DEC1 but decreased those of DEC2 in PC‑3 cells. Moreover, TGF‑β evoked the phosphorylation of Smad2, followed by the activation of mesenchymal markers, such as N‑cadherin and vimentin, in addition to the suppression of epithelial markers, such as E‑cadherin. The knockdown of DEC1 restrained TGF‑β‑induced cell morphology changes as well as cell motility, which was compatible with the upregulation of E‑cadherin and downregulation of pSmad2, N‑cadherin, and vimentin. However, DEC2 knockdown endorsed PC‑3 cells with a more metastatic phenotype. EMT‑related markers in DEC2 siRNA‑transfected cells exhibited a reverse expression pattern when compared with that in DEC1 siRNA‑transfected cells. Taken together, these results provide evidence that DEC1 and DEC2 have opposite effects on TGF‑β‑induced EMT in human prostate cancer PC‑3 cells.

Indexed as

Epithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticBasic Helix-Loop-Helix ProteinsCell Line, TumorCell MovementGene Knockdown TechniquesHumansMaleProstatic NeoplasmsTransforming Growth Factor betaTumor Suppressor ProteinsBasic Helix-Loop-Helix ProteinsBHLHE41 protein, humanDELEC1 protein, humanTransforming Growth Factor betaTumor Suppressor Proteins

Identifiers

PMID30106153
PMCPMC6131663
OpenAlexW2886940025

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.