Evidence map›Paper›PMID 24157866›Full record

ArticleCell death & disease2013

Tumor suppressor PDCD4 modulates miR-184-mediated direct suppression of C-MYC and BCL2 blocking cell growth and survival in nasopharyngeal carcinoma.

Yan Zhen, Zhen Liu, Huiling Yang, Xiaoli Yu, Qiangyun Wu, Shengni Hua, Xiaobin Long, Qingping Jiang, Ye Song, Chao Cheng and 9 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed, 3 pooled it
5.9field-weighted citation impact, top 3% 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

86 citing papers in PubMed, 3 syntheses or guidelines pooled it, 128 citations in OpenAlex.

  1. Pooled it
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  4. Article
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  9. IncreasedThe Journal of international medical research · 2024
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  10. Review
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  15. Article
  16. Functional Roles of JNK and p38 MAPK Signaling in Nasopharyngeal Carcinoma.International journal of molecular sciences · 2022
    Review
  17. Review
  18. PIK-75 overcomes venetoclax resistanceAmerican journal of cancer research · 2022
    Article
  19. Article
  20. Review

26 more citing papers are in PubMed but not listed here.

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

19 authors at 4 institutions in 1 country.

Yan Zhen1] Department of Pathology, Basic School, Guangzhou Medical University, Guangzhou 510182, PR China [2] Cancer Research Institute, Southern Medical University, Guangzhou 510515, PR China [3] Institute of Respiratory Diseases, Affiliated Hospital of Guangdong Medical College, Zhanjiang 524000, PR China.
Zhen Liu
Huiling Yang
Xiaoli Yu
Qiangyun Wu
Shengni Hua
Xiaobin Long
Qingping Jiang
Ye Song
Chao Cheng
Hao Wang
Menyang Zhao
Qiaofen Fu
Xiaoming Lyu
Yiyu Chen
Yue Fan
Yan Liu
Xin Li
Weiyi Fang
Southern Medical University · CNGuangzhou Medical University · CNGuangdong Medical College · CNZhujiang Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Programmed cell death 4 (PDCD4), a novel tumor suppressor, inhibits cell proliferation, migration and invasion as well as promotes cell apoptosis in tumors. However, the molecular mechanism of its tumor-suppressive function remains largely unknown in tumors including nasopharyngeal carcinoma (NPC). In this study, downregulated PDCD4 expression was significantly associated with the status of NPC progression and poor prognosis. PDCD4 markedly suppressed the ability of cell proliferation and cell survival by modulating C-MYC-controlled cell cycle and BCL-2-mediated mitochondrion apoptosis resistance signals, and oncogenic transcription factor C-JUN in NPC. Furthermore, miR-184, a tumor-suppressive miRNA modulated by PDCD4 directly targeting BCL2 and C-MYC, participated in PDCD4-mediated suppression of cell proliferation and survival in NPC. Further, we found that PDCD4 decreased the binding of C-Jun to the AP-1 element on the miR-184 promoter regions by PI3K/AKT/JNK/C-Jun pathway and stimulated miR-184 expression. In clinical fresh specimens, reduced PDCD4 mRNA level was positively correlated with miR-184 expression in NPC. Our studies are the first to demonstrate that PDCD4 as tumor suppressor regulated miR-184-mediated direct targeting of BCL2 and C-MYC via PI3K/AKT and JNK/C-Jun pathway attenuating cell proliferation and survival in NPC.

Indexed as

AdultAgedAged, 80 and overApoptosisApoptosis Regulatory ProteinsCarcinomaCell CycleCell ProliferationCell SurvivalDisease ProgressionDown-RegulationFemaleGene Expression Regulation, NeoplasticHumansJNK Mitogen-Activated Protein KinasesMaleApoptosis Regulatory ProteinsJNK Mitogen-Activated Protein KinasesMicroRNAsMIRN184 microRNA, humanPDCD4 protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2Proto-Oncogene Proteins c-junProto-Oncogene Proteins c-mycRNA-Binding Proteins

Identifiers

PMID24157866
PMCPMC3824685
OpenAlexW1972371148

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.