Evidence map›Paper›PMID 26261528›Full record

ArticleInternational journal of clinical and experimental pathology2015

Unfolded protein response mediated JNK/AP-1 signal transduction, a target for ovarian cancer treatment.

Gao-Feng Zheng, Zhen Cai, Xiang-Kai Meng, Yi Zhang, Wei Zhu, Xiao-Yan Pang, Lei Dou

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

15 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Review
  3. Withaferin A and Celastrol Overwhelm Proteostasis.International journal of molecular sciences · 2023
    Review
  4. JNK signaling as a target for anticancer therapy.Pharmacological reports : PR · 2021
    Review
  5. Review
  6. Review
  7. Review
  8. Glutathione in Ovarian Cancer: A Double-Edged Sword.International journal of molecular sciences · 2018
    Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. 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 2 institutions in 1 country.

Gao-Feng ZhengThe Bone Marrow Transplantation Center & Multiple Myeloma Treatment Center, The First Affiliated Hospital of Medical College, Zhejiang University Hangzhou 310003, Zhejiang, China.
Zhen CaiThe Bone Marrow Transplantation Center & Multiple Myeloma Treatment Center, The First Affiliated Hospital of Medical College, Zhejiang University Hangzhou 310003, Zhejiang, China.
Xiang-Kai MengDepartment of Gynecology, The First Hospital of China Medical University Shenyang 110001, Liaoning, China.
Yi ZhangDepartment of Gynecology, The First Hospital of China Medical University Shenyang 110001, Liaoning, China.
Wei ZhuDepartment of Gynecology, The First Hospital of China Medical University Shenyang 110001, Liaoning, China.
Xiao-Yan PangDepartment of Gynecology, The First Hospital of China Medical University Shenyang 110001, Liaoning, China.
Lei DouDepartment of Gynecology, The First Hospital of China Medical University Shenyang 110001, Liaoning, China.
First Hospital of China Medical University · CNFirst Affiliated Hospital Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Researches have revealed several stressors, which could activate unfolded protein response (UPR) in cells. However, the survival or death pathway was determined by the duration of UPR exposure. Based on the UPR mediated death pathway, our study was aimed to investigate role of UPR on c-Jun N-terminal kinase (JNK)/activator protein-1 (Ap-1) signal transduction in diindolylmethane (DIM) treated ovarian cancer cell lines. Activation of UPR proteins, UPR mediated apoptotic signaling proteins and expression level of EpCAM, JNK, Ap-1, Caspase-3 and Bcl-2 were measured. Protein and gene expression, transcription factor activity, and protein phosphorylation were measured using standard molecular biology techniques. Our results demonstrated DIM treatment had significantly increased the expression of Endoplasmic reticulum (ER) stress regulators such as Bip, IRE1, CHOP and activation of UPR related apoptotic proteins in ovarian cancer cells. Decreased expression of EpCAM and activity of AP-1 transcription factor were observed in DIM treated cells. The pharmacologic inhibitors of the JNK signal transduction pathway, suggest that the impact of EpCAM expression on AP-1 transcription factor activity is mediated through the JNK pathway. Taken together, these results suggest that UPR mediated JNK/Ap-1 signal transduction has a significant role in the regulation of apoptosis in human ovarian cancer cells, and is a potential molecular target to enhance sensitivity of ovarian cancer to chemotherapy.

Indexed as

Antigens, NeoplasmAntineoplastic AgentsAutophagyCaspase 3Cell Adhesion MoleculesCell Line, TumorDose-Response Relationship, DrugEndoplasmic ReticulumEpithelial Cell Adhesion MoleculeFemaleHumansIndolesJNK Mitogen-Activated Protein KinasesMolecular Targeted TherapyOvarian NeoplasmsProtein Kinase Inhibitors3,3'-diindolylmethaneAntigens, NeoplasmAntineoplastic AgentsBCL2 protein, humanCASP3 protein, humanCaspase 3Cell Adhesion MoleculesEPCAM protein, humanEpithelial Cell Adhesion MoleculeIndolesJNK Mitogen-Activated Protein KinasesProtein Kinase InhibitorsProto-Oncogene Proteins c-bcl-2Transcription Factor AP-1diindolylmethaneendoplasmic reticulum stressEpCAMSKOV3 cells

Identifiers

PMID26261528
PMCPMC4525862
OpenAlexW2475331421

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.