Evidence map›Paper›PMID 27471108›Full record

ArticleNeuro-oncology2017

miR-423-5p contributes to a malignant phenotype and temozolomide chemoresistance in glioblastomas.

Shouwei Li, Ailiang Zeng, Qi Hu, Wei Yan, Yanwei Liu, Yongping You

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neuro-oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
–field-weighted citation impact
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

75 citing papers in PubMed.

  1. Review
  2. Tumor heterogeneity and resistance in glioblastoma: the role of stem cells.Apoptosis : an international journal on programmed cell death · 2025
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  18. MiR-423-5p prevents MALAT1-mediated proliferation and metastasis in prostate cancer.Journal of experimental & clinical cancer research : CR · 2022
    Article
  19. Article
  20. Review

15 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

6 authors.

Shouwei LiDepartment of Neurosurgery, Sanbo Brain Hospital, Capital Medical University, Beijing, China (S.L.); Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China (A.Z., Q.H., W.Y., Y.Y.); Beijing Neurosurgical Institute, Capital Medical University, Beijing, China (Y.L.).
Ailiang ZengDepartment of Neurosurgery, Sanbo Brain Hospital, Capital Medical University, Beijing, China (S.L.); Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China (A.Z., Q.H., W.Y., Y.Y.); Beijing Neurosurgical Institute, Capital Medical University, Beijing, China (Y.L.).
Qi HuDepartment of Neurosurgery, Sanbo Brain Hospital, Capital Medical University, Beijing, China (S.L.); Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China (A.Z., Q.H., W.Y., Y.Y.); Beijing Neurosurgical Institute, Capital Medical University, Beijing, China (Y.L.).
Wei YanDepartment of Neurosurgery, Sanbo Brain Hospital, Capital Medical University, Beijing, China (S.L.); Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China (A.Z., Q.H., W.Y., Y.Y.); Beijing Neurosurgical Institute, Capital Medical University, Beijing, China (Y.L.).
Yanwei LiuDepartment of Neurosurgery, Sanbo Brain Hospital, Capital Medical University, Beijing, China (S.L.); Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China (A.Z., Q.H., W.Y., Y.Y.); Beijing Neurosurgical Institute, Capital Medical University, Beijing, China (Y.L.).
Yongping YouDepartment of Neurosurgery, Sanbo Brain Hospital, Capital Medical University, Beijing, China (S.L.); Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China (A.Z., Q.H., W.Y., Y.Y.); Beijing Neurosurgical Institute, Capital Medical University, Beijing, China (Y.L.).

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGliomas are based on a genetic abnormality and present with a dismal prognosis. MicroRNAs (miRNAs) are considered to be important mediators of gene expression in glioma tissues.

methodsReal-time PCR was used to analyze the expression of microRNA-423-5p (miR-423-5p) in human glioma samples and normal brain tissue. Apoptosis, cell cycle, proliferation, immunostaining, transwell, in vitro 2D and 3D migration, and chemosensitivity assays were performed to assess the phenotypic changes in glioma cells overexpressing miRNA-423-5p. Western blotting was used to determine the expression of inhibitor of growth 4 (ING-4)in glioma tissues, and a luciferase reporter assay was conducted to confirm whether ING-4 is a direct target of miR-423-5p. Western blotting was used to identify the potential signaling pathways that are affected in glioma cell growth by miR-423-5p. Xenograft tumors were examined in vivo for the carcinogenic effects of miR-423-5p in glioma tissues.

resultsWe first reported that miR-423-5p expression was increased in gliomas and was a potential tumor promoter via targeting ING-4. The overexpression of miR-423-5p resulted in upregulation of important signaling molecules such as p-AKT and p-ERK1/2. In clinical samples, miR-423-5p was dysregulated, and a corresponding alteration in ING-4 expression was observed (P = .0207). Furthermore, the overexpression of miR-423-5p strengthened glioma cell proliferation, angiogenesis, and invasion. Finally, miR-423-5p overexpression also strengthened GBM neurosphere formation and rendered glioma cells resistant to temozolomide (TMZ).

conclusionThis study establishes that miR-423-5p functions as an oncogene in glioma tissues by suppressing ING-4 and suggests that it has therapeutic potential for glioma.

Indexed as

AnimalsAntineoplastic Agents, AlkylatingApoptosisBrain NeoplasmsCell Cycle ProteinsCell ProliferationDacarbazineDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticGlioblastomaHomeodomain ProteinsHumansMaleMiceMice, Inbred BALB CMice, NudeAKT1 protein, humanAntineoplastic Agents, AlkylatingCell Cycle ProteinsDacarbazineHomeodomain ProteinsING4 protein, humanMAPK1 protein, humanMicroRNAsMIRN423 microRNA, humanMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Proto-Oncogene Proteins c-aktTemozolomideTumor Suppressor ProteinschemoresistancegliomaING-4miR-423-5p

Identifiers

PMID27471108
PMCPMC5193021

What OpenQuestion holds

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Registered trials

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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.