Evidence map›Paper›PMID 25823655›Full record

ArticleOncotarget2015

miR-93 promotes cell proliferation in gliomas through activation of PI3K/Akt signaling pathway.

Lili Jiang, Chanjuan Wang, Fangyong Lei, Longjuan Zhang, Xin Zhang, Aibin Liu, Geyan Wu, Jinrong Zhu, Libing Song

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed, 1 pooled it
6.4field-weighted citation impact, top 2% 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

65 citing papers in PubMed, 1 synthesis or guideline pooled it, 111 citations in OpenAlex.

  1. Pooled it
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  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
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  11. Article
  12. MiRNA-93: a novel signature in human disorders and drug resistance.Cell communication and signaling : CCS · 2023
    Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. miR-451 suppresses EMT and metastasis in glioma cells.Cell cycle (Georgetown, Tex.) · 2021
    Article
  20. Article

5 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

9 authors at 4 institutions in 1 country.

Lili JiangDepartment of Pathophysiology, Guangzhou Medical University, Guangzhou 510182, China.
Chanjuan WangDepartment of the Central Laboratory, The First Affiliated Hospital/School of Clinical Medicine of Guangdong Pharmaceutical University, Guangzhou 510080, China.
Fangyong LeiState Key Laboratory of Oncology in Southern China, Department of Experimental Research, Cancer Centre, Sun Yat-sen University, Guangzhou 510060, China.
Longjuan ZhangLaboratory of Surgery, First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, China.
Xin ZhangState Key Laboratory of Oncology in Southern China, Department of Experimental Research, Cancer Centre, Sun Yat-sen University, Guangzhou 510060, China.
Aibin LiuDepartment of Biochemistry, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong 510080, China.
Geyan WuDepartment of Biochemistry, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong 510080, China.
Jinrong ZhuDepartment of Biochemistry, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong 510080, China.
Libing SongState Key Laboratory of Oncology in Southern China, Department of Experimental Research, Cancer Centre, Sun Yat-sen University, Guangzhou 510060, China.
Sun Yat-sen University · CNSun Yat-sen University Cancer Center · CNGuangdong Pharmaceutical University · CNThe First Affiliated Hospital, Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The PI3K/Akt signaling pathway is frequently activated in various human cancer types and plays essential roles in development and progression of cancers. Multiple regulators, such as phosphatase and tensin homolog (PTEN) and PH domain leucine rich repeat protein phosphatases (PHLPP), have also found to be involved in suppression of the PI3K/Akt signaling pathway. However, how suppressive effects mediated by these regulators are concomitantly disrupted in cancers, which display constitutively activated PI3K/Akt signaling, remains puzzling. In the present study, we reported that the expression of miR-93 was markedly upregulated in glioma cell lines and clinical glioma tissues. Statistical analysis revealed that miR-93 levels significantly correlated with clinicopathologic grade and overall survival in gliomas. Furthermore, we found that overexpressing miR-93 promoted, but inhibition of miR-93 reduced, glioma cell proliferation and cell-cycle progression. We demonstrated that miR-93 activated PI3K/Akt signaling through directly suppressing PTEN, PHLPP2 and FOXO3 expression via targeting their 3'UTRs. Therefore, our results suggest that miR-93 might play an important role in glioma progression and uncover a novel mechanism for constitutive PI3K/Akt activation in gliomas.

Indexed as

Brain NeoplasmsCell CycleCell Line, TumorCell ProliferationGliomaHumansMicroRNAsPhosphatidylinositol 3-KinasesPrognosisProto-Oncogene Proteins c-aktSignal TransductionUp-RegulationMicroRNAsMIRN93 microRNA, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktgliomasmiR-93PI3K/Akt

Identifiers

PMID25823655
PMCPMC4480752
OpenAlexW2167865100

What OpenQuestion holds

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LicenceCC BY
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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.