Evidence map›Paper›PMID 32214825›Full record

ArticleOncoTargets and therapy2020

Tumor Suppressor microRNA-138 Suppresses Low-Grade Glioma Development and Metastasis via Regulating IGF2BP2.

Yang Yang, Xinyu Liu, Lulu Cheng, Li Li, Zhenyu Wei, Zong Wang, Gang Han, Xuefeng Wan, Zaizhong Wang, Jianhua Zhang and 1 more

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

23 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. IMPlications of IMP2 in RNA Biology and Disease.International journal of molecular sciences · 2025
    Review
  4. Review
  5. Article
  6. Article
  7. The Role of miR-138 in Cardiovascular Diseases.BioMed research international · 2025
    Review
  8. IGF2BPs as novel mGenes & diseases · 2024
    Review
  9. Article
  10. Article
  11. Article
  12. Article
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  14. Article
  15. Review
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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

11 authors at 4 institutions in 1 country.

Yang Yang *Henan Key Laboratory for Medical Imaging of Neurological Diseases, People's Hospital of Zhengzhou University, Zhengzhou 450003, People's Republic of China.
Xinyu Liu *School of Intelligent Manufacturing, The Huanghuai University, Zhumadian 463000, People's Republic of China.
Lulu ChengDepartment of Neurosurgery, Zhumadian Central Hospital, Zhumadian 463000, People's Republic of China.
Li LiDepartment of Neurosurgery, Zhumadian Central Hospital, Zhumadian 463000, People's Republic of China.
Zhenyu WeiDepartment of Neurosurgery, Second Affiliated Hospital of Xinxiang Medical College, Xinxiang 453000, People's Republic of China.
Zong WangDepartment of Neurosurgery, Zhumadian Central Hospital, Zhumadian 463000, People's Republic of China.
Gang HanDepartment of Neurosurgery, Zhumadian Central Hospital, Zhumadian 463000, People's Republic of China.
Xuefeng WanDepartment of Neurosurgery, Zhumadian Central Hospital, Zhumadian 463000, People's Republic of China.
Zaizhong WangDepartment of Neurosurgery, Zhumadian Central Hospital, Zhumadian 463000, People's Republic of China.
Jianhua ZhangMedical Engineering Technology and Data Mining Institute of Zhengzhou University, Zhengzhou 450000, People's Republic of China.
Chuanliang ChenHenan Key Laboratory for Medical Imaging of Neurological Diseases, People's Hospital of Zhengzhou University, Zhengzhou 450003, People's Republic of China.
Zhumadian Central Hospital · CNZhengzhou University · CNHenan Psychiatric Hospital · CNHuanghuai University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLow-grade gliomas (LGG), approximately constitute one-third of all types of gliomas, are prone to relapse and metastasis. MicroRNA-138 (miR-138) is reported to be dysregulated in diverse human tumors and mainly function as a tumor suppressor. In this study, we analyzed the expression profile and function of miR-138 in LGG.

methodsQuantitative PCR (qPCR) and public database bioinformatics analysis were performed to determine the miR-138 levels in LGG. MiR-138 overexpression in LGG cells was achieved by miR-138 mimics transfection. Cell proliferation was assessed by CCK8, EdU and colony formation assays. Cell invasion and migration were analyzed by transwell and wound-healing assays. Xenograft model was employed to study the role of miR-138 in LGG growth in vivo. The target of miR-138 was validated by multiple methods, such as luciferase reporter assay, RT-qPCR and Western blot. Bioinformatics analysis was conducted to explore the molecular mechanisms by which miR-138 contributed to LGG progression.

resultsmiR-138 was significantly downregulated in LGG tumor tissues and low expression of miR-138 was significantly associated with poor prognosis as well as relapse and metastasis in LGG patients. Functional analysis indicated that ectopic miR-138 expression suppressed LGG cell growth and invasive phenotype in vitro, and inhibited tumor development in vivo. Moreover, miR-138 directly targeted and repressed insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2) by targeting the 3'-UTR of IGF2BP2, inhibiting epithelial to mesenchymal transition (EMT) to attenuate LGG aggressiveness. In addition, we found that elevated IGF2BP2 expression correlates with poor survival of LGG patients.

conclusionmiR-138 may function as a tumor inhibitor by directly inhibiting IGF2BP2 and suppressing EMT in the progression of LGG.

Indexed as

EMTIGF2BP2LGGmiR-138tumor prognosis

Identifiers

PMID32214825
PMCPMC7082711
OpenAlexW3011862050

What OpenQuestion holds

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LicenceCC BY-NC
Read underepoch 390

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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.