Evidence map›Paper›PMID 31060254›Full record

ArticleInternational journal of molecular sciences2019

Glycidamide Promotes the Growth and Migratory Ability of Prostate Cancer Cells by Changing the Protein Expression of Cell Cycle Regulators and Epithelial-to-Mesenchymal Transition (EMT)-Associated Proteins with Prognostic Relevance.

Titus Ime Ekanem, Chi-Chen Huang, Ming-Heng Wu, Ding-Yen Lin, Wen-Fu T Lai, Kuen-Haur Lee

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Assessment of the genotoxicity of acrylamide.EFSA journal. European Food Safety Authority · 2022
    Article
  6. Article
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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

6 authors at 3 institutions in 3 countries.

Titus Ime EkanemPh.D. Program for Cancer Molecular Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University and Academia Sinica, Taipei 11529, Taiwan. titusekanem@yahoo.com.
Chi-Chen HuangGraduate Institute of Neural Regenerative Medicine, College of Medical Science and Technology, Taipei Medical University, Taipei 11031, Taiwan. hcc0609@tmu.edu.tw.
Ming-Heng WuGraduate Institute of Translational Medicine, Taipei Medical University, Taipei 11031, Taiwan. mhwu1015@tmu.edu.tw.
Ding-Yen LinDepartment of Biotechnology and Bioindustry Sciences, College of Bioscience and Biotechnology, National Cheng Kung University, Tainan 003107, Taiwan. lindy@mail.ncku.edu.tw.
Wen-Fu T LaiMcLean Imaging Center, McLean Hospital, Harvard Medical School, Belmont, MA 02478, USA. laitw@tmu.edu.tw.
Kuen-Haur LeeGraduate Institute of Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei 11031, Taiwan. khlee@tmu.edu.tw.
Taipei Medical University · TWHarvard University · USUniversity of Uyo · NG

Funding

Health and welfare surcharge of tobacco products of Taiwan MOHW108-TDU-B-212-124020Ministry of Education of Taiwan DP2-107-21121-02-C-03
6 · The paper itself

Abstract

Acrylamide (AA) and glycidamide (GA) can be produced in carbohydrate-rich food when heated at a high temperature, which can induce a malignant transformation. It has been demonstrated that GA is more mutagenic than AA. It has been shown that the proliferation rate of some cancer cells are increased by treatment with GA; however, the exact genes that are induced by GA in most cancer cells are not clear. In the present study, we demonstrated that GA promotes the growth of prostate cancer cells through induced protein expression of the cell cycle regulator. In addition, we also found that GA promoted the migratory ability of prostate cancer cells through induced epithelial-to-mesenchymal transition (EMT)-associated protein expression. In order to understand the potential prognostic relevance of GA-mediated regulators of the cell cycle and EMT, we present a three-gene signature to evaluate the prognosis of prostate cancer patients. Further investigations suggested that the three-gene signature (CDK4, TWIST1 and SNAI2) predicted the chances of survival better than any of the three genes alone for the first time. In conclusion, we suggested that the three-gene signature model can act as marker of GA exposure. Hence, this multi-gene panel may serve as a promising outcome predictor and potential therapeutic target in prostate cancer patients.

Indexed as

Gene Expression Regulation, NeoplasticBiomarkers, TumorCell CycleCell Cycle ProteinsCell Line, TumorCell MovementCell SurvivalEpithelial-Mesenchymal TransitionEpoxy CompoundsGene Expression ProfilingHumansKaplan-Meier EstimateMalePrognosisProstatic NeoplasmsSignal TransductionBiomarkers, TumorCell Cycle ProteinsEpoxy Compoundsglycidamidecell cycle regulatorEMTgene signatureglycidamideprognosisprostate cancer

Identifiers

PMID31060254
PMCPMC6540322
OpenAlexW2942951264

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.