Evidence map›Paper›PMID 30013652›Full record

ArticleOncology letters2018

Juglone suppresses epithelial-mesenchymal transition in prostate cancer cells via the protein kinase B/glycogen synthase kinase-3β/Snail signaling pathway.

Fang Fang, Shuang Chen, Jing Ma, Jiabo Cui, Qiang Li, Guixian Meng, Liguo Wang

Open access · diamondAbstract read
In one paragraph

Article in Oncology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

20 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. [Juglone induces proliferation inhibition and apoptosis of cervical cancer cellsNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. Juglone in Oxidative Stress and Cell Signaling.Antioxidants (Basel, Switzerland) · 2019
    Review
  20. Review
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.

Fang FangDepartment of Immunology, Jilin Medical University, Jilin City, Jilin 132013, P.R. China.
Shuang ChenDepartment of Immunology, Jilin Medical University, Jilin City, Jilin 132013, P.R. China.
Jing MaDepartment of Immunology, Jilin Medical University, Jilin City, Jilin 132013, P.R. China.
Jiabo CuiDepartment of Immunology, Jilin Medical University, Jilin City, Jilin 132013, P.R. China.
Qiang LiDepartment of Immunology, Jilin Medical University, Jilin City, Jilin 132013, P.R. China.
Guixian MengDepartment of Immunology, Jilin Medical University, Jilin City, Jilin 132013, P.R. China.
Liguo WangDepartment of Urology Surgery, Affiliated Hospital of Jilin Medical University, Jilin City, Jilin 132013, P.R. China.
Jilin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial-mesenchymal transition (EMT) serves an important role in the metastasis of prostate cancer. Juglone is a natural compound isolated from plants that is reported to possess potent cytotoxic properties. However, there are no studies on the anti-EMT effect of juglone in prostate cancer, or its potential underlying mechanisms of action. In the present study, the effect of juglone on the EMT of prostate cancer cells was investigated. Transwell assays were used to demonstrate that juglone inhibits the migration and invasion of the prostate cancer (PC) LNCaP and LNCaP-AI cell lines. Results from western blot analysis demonstrated that juglone increases the expression of the epithelial marker E-cadherin while decreasing the expression of mesenchymal markers (N-cadherin and Vimentin) in a dose-dependent manner. The data from the present study also revealed that juglone downregulates the expression of Snail, a repressor of E-cadherin and an inducer of EMT. Furthermore, juglone prevented inactivation of glycogen synthase kinase-3β (GSK-3β), an endogenous inhibitor of Snail in a dose-dependent manner. Lithium chloride (LiCl), a GSK-3β inhibitor, prevented juglone-mediated downregulation of Snail expression and upregulation of E-cadherin. In addition, phosphorylation and subsequent activation of protein kinase B (Akt), which is known to phosphorylate GSK-3β at serine 9 (Ser9), leading to its inhibition, were significantly decreased by juglone in LNCaP and LNCaP-AI cells. Inhibition of the phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/Akt pathway by LY294002 augmented juglone-mediated GSK-3β activity by inhibiting Ser9 phosphorylation. These findings indicated that juglone suppresses EMT via the Akt/GSK-3β/Snail pathway, consequently decreasing the invasiveness of PC cells.

Indexed as

epithelial-mesenchymal transitionglycogen synthase kinase-3βjuglonemetastasisprostate cancerprotein kinase BSnail

Identifiers

PMID30013652
PMCPMC6036567
OpenAlexW2805895003

What OpenQuestion holds

Textmetadata
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.