Evidence map›Paper›PMID 32158359›Full record

ArticleCancer cell international2020

MiR-181b suppress glioblastoma multiforme growth through inhibition of SP1-mediated glucose metabolism.

JianXing Yin, ZhuMei Shi, WenJin Wei, Chenfei Lu, Yutian Wei, Wei Yan, Rui Li, JunXia Zhang, YongPing You, XieFeng Wang

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing 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

25 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Unraveling the role of specificity protein 1 in gliomas: pathophysiology and clinical implications.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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  13. Connexins and Glucose Metabolism in Cancer.International journal of molecular sciences · 2022
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  14. SP and KLF Transcription Factors in Cancer Metabolism.International journal of molecular sciences · 2022
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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

10 authors at 2 institutions in 1 country.

JianXing Yin *1Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
ZhuMei Shi *1Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
WenJin Wei *2Department of Neurosurgery, The Affiliated Ganzhou Hospital of Nanchang University, 16 Meiguan Avenue, Ganzhou, 341000 Jiangxi China.
Chenfei Lu *1Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Yutian Wei1Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Wei Yan1Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Rui Li1Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
JunXia Zhang1Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
YongPing You1Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
XieFeng Wang1Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.ORCID 0000-0001-7031-5532
Jiangsu Province Hospital · CNNanchang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGlucose metabolic reprogramming is a significant hallmark of malignant tumors including GBM. Previous studies suggest that microRNAs play key roles in modulating this process in GBM cells. miR-181b acts as a tumor suppressor miRNA in influencing glioma tumorigenesis. Our previous results showed that miR-181b was down-regulated in glioma cells and tissues.

methodsThe extracellular acidification rate (ECAR), colony formation assay and levels of Glut1 and PKM2 were measured to assess the glucose metabolic and proliferation changes in GBM cells overexpressing miR-181b. Immunoblotting and luciferase reporter assay were performed to confirm the expression and role of SP1 as a direct target of miR-181b. ChIP assay was used to figure out the transcriptional regulation of SP1 on Glut1 and PKM2. In vivo study was examined for the role of miR-181b in GBM cells.

resultsMiR-181b overexpression significantly reduced the glucose metabolic and colony formation ability of GBM cells. And, SP1 was confirmed as a direct target of miR-181b while upregulation of SP1 could reverse the influence of overexpression of miR-181b. Furthermore, Glut1 and PKM2 could be regulated by SP1. Finally, miR-181b could inhibit the tumor growth in vivo.

conclusionsOur article demonstrated the inhibitory effect of miR-181b on glucose metabolism and proliferation in GBM by suppressing SP1 expression.

Indexed as

GliomaGlucose metabolismmiR-181bSP1

Identifiers

PMID32158359
PMCPMC7057587
OpenAlexW3011453217

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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.