Evidence map›Paper›PMID 24566468›Full record

ArticleOncotarget2014

Cytotoxic effects of 15d-PGJ2 against osteosarcoma through ROS-mediated AKT and cell cycle inhibition.

Chueh-Chuan Yen, Chung-Der Hsiao, Wei-Ming Chen, Yao-Shan Wen, Yung-Chan Lin, Ting-Wei Chang, Fang-Yi Yao, Shih-Chieh Hung, Jir-You Wang, Jen-Hwey Chiu and 7 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.1field-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

23 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. 15d-PGJInternational journal of molecular sciences · 2021
    Article
  7. Article
  8. Review
  9. 15-Deoxy-ΔJournal of cancer prevention · 2020
    Article
  10. 15-Deoxy-ΔDrug design, development and therapy · 2019
    Review
  11. Article
  12. 15d-PGJ2 is a new hope for controlling tumor growth.American journal of translational research · 2018
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

17 authors at 6 institutions in 2 countries.

Chueh-Chuan YenDivision of Hematology and Oncology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan.
Chung-Der Hsiao
Wei-Ming Chen
Yao-Shan Wen
Yung-Chan Lin
Ting-Wei Chang
Fang-Yi Yao
Shih-Chieh Hung
Jir-You Wang
Jen-Hwey Chiu
Hsei-Wei Wang
Chi-Hung Lin
Tain-Hsiung Chen
Paul Chih-Hsueh Chen
Chien-Lin Liu
Cheng-Hwai Tzeng
Jonathan A Fletcher
Taipei Veterans General Hospital · TWNational Yang Ming Chiao Tung University · TWNational Yang Ming Chiao Tung University · TWTaipei City Hospital · TWBrigham and Women's Hospital · USChung Yuan Christian University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Polo-like kinase 1 (PLK1), a critical cell cycle regulator, has been identified as a potential target in osteosarcoma (OS). 15-deoxy-Δ12, 14-prostaglandin J2 (15d-PGJ2), a prostaglandin derivative, has shown its anti-tumor activity by inducing apoptosis through reactive oxygen species (ROS)-mediated inactivation of v-akt, a murine thymoma viral oncogene homolog, (AKT) in cancer cells. In the study analyzing its effects on arthritis, 15d-PGJ2 mediated shear-induced chondrocyte apoptosis via protein kinase A (PKA)-dependent regulation of PLK1. In this study, the cytotoxic effect and mechanism underlying 15d-PGJ2 effects against OS were explored using OS cell lines. 15d-PGJ2 induced significant G2/M arrest, and exerted time- and dose-dependent cytotoxic effects against all OS cell lines. Western blot analysis showed that both AKT and PKA-PLK1 were down-regulated in OS cell lines after treatment with 15d-PGJ2. In addition, transfection of constitutively active AKT or PLK1 partially rescued cells from 15d-PGJ2-induced apoptosis, suggesting crucial roles for both pathways in the anti-cancer effects of 15d-PGJ2. Moreover, ROS generation was found treatment with 15d-PGJ2, and its cytotoxic effect could be reversed with N-acetyl-l-cysteine. Furthermore, inhibition of JNK partially rescued 15d-PGJ2 cytotoxicity. Thus, ROS-mediated JNK activation may contribute to apoptosis through down-regulation of the p-Akt and PKA-PLK1 pathways. 15d-PGJ2 is a potential therapeutic agent for OS, exerting cytotoxicity mediated through both AKT and PKA-PLK1 inhibition, and these results form the basis for further analysis of its role in animal studies and clinical applications.

Indexed as

ApoptosisBone NeoplasmsCell CycleCell Cycle ProteinsCell Growth ProcessesCell Line, TumorDown-RegulationG2 Phase Cell Cycle CheckpointsHumansJNK Mitogen-Activated Protein KinasesM Phase Cell Cycle CheckpointsOsteosarcomaPhosphorylationPolo-Like Kinase 1Prostaglandin D2Protein Serine-Threonine Kinases15-deoxy-delta(12,14)-prostaglandin J2Cell Cycle ProteinsJNK Mitogen-Activated Protein KinasesPolo-Like Kinase 1Prostaglandin D2Protein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktReactive Oxygen Species

Identifiers

PMID24566468
PMCPMC3996657
OpenAlexW2154932244

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.