Evidence map›Paper›PMID 33911899›Full record

ArticleCancer management and research2021

LncRNA MAFG-AS1 Suppresses the Maturation of miR-34a to Promote Glioblastoma Cell Proliferation.

Hao Zhao, Jun Li, Xin Yan, Xinchao Bian

Abstract read
In one paragraph

Article in Cancer management and research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
–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

12 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. [Effect of LncRNA DANCR on the immune microenvironment of glioma cells by regulating the miR-656/BMPR1A axis].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2026
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  7. Carcinogenic roles of MAFG-AS1 in human cancers.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024
    Review
  8. LncRNA MAFG-AS1 is involved in human cancer progression.European journal of medical research · 2023
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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

4 authors.

Hao ZhaoDepartment of Neurosurgery, Zibo Central Hospital, Zibo City, Shandong Province, 255036, People's Republic of China.
Jun LiDepartment of Neurosurgery, Zibo Central Hospital, Zibo City, Shandong Province, 255036, People's Republic of China.
Xin YanDepartment of Ultrasound, Central Hospital Affiliated to Shandong University, Zibo City, Shandong Province, 255036, People's Republic of China.
Xinchao BianDepartment of Neurosurgery, Zibo Central Hospital, Zibo City, Shandong Province, 255036, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeLncRNA MAFG-AS1 plays critical roles in several types of cancer, while its role in glioblastoma (GBM) is unknown. By analyzing the TCGA dataset, we observed the upregulation of MAFG-AS1 in GBM. This study aimed to investigate the involvement of MAFG-AS1 in GBM cancer.

methodsThe expression levels of MAFG-AS1, mature miR-34a, and miR-34a precursor in GBM and paired non-tumor tissues of 56 GBM patients were determined by RT-qPCR. Correlations are analyzed using linear regression. Overexpression of MAFG-AS1 was achieved in GBM cells, followed by measurement of the expression levels of mature miR-34a, miR-34a precursor, DICER and Drosha by RT-qPCR. The roles of MAFG-AS1 and miR-34a in regulating GBM cell proliferation were evaluated by CCK-8 assay. Flow cytometry was performed to explore the role of MAFG-AS1 and miR-34a in regulating the apoptosis and cell cycle of GBM cells. Cell scratch experiment was performed to determine the role of MAFG-AS1 and miR-34a in regulating the migration of GBM cells. Subcutaneous tumor animal model was used for in vivo study. The expressions levels of BCL-2 and caspase-3 were detected by Western blot analysis.

resultsMAFG-AS1 was upregulated in GBM, while mature miR-34a was downregulated in GBM. Interestingly, MAFG-AS1 was inversely correlated with mature miR-34a but not miR-34a precursor across GBM tissues. In GBM tissues, the overexpression of MAFG-AS1 did not affect the expression levels of miR-34a precursor but reduced the expression levels of mature miR-34a. MAFG-AS1 promoted the expression of DICER and Drosha in GBM cells. Moreover, the overexpression of MAFG-AS1 promoted the proliferation of GBM cells and reduced the inhibitory effects of miR-34a on cell proliferation but did not affect cell cycle, apoptosis and migration. The overexpression of MAFG-AS1 promoted the progression of GBM in vivo by promoting the proliferation of GBM cells while miR-34a reversed the effect of overexpression of MAFG-AS1.

conclusionsMAFG-AS1 may suppress the maturation of miR-34a to promote GBM cell proliferation.

Indexed as

glioblastomaMAFG-AS1maturationmiR-34a

Identifiers

PMID33911899
PMCPMC8075183

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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.