Evidence map›Paper›PMID 33718112›Full record

ArticleFrontiers in oncology2020

Hypoxia-Induced miR-137 Inhibition Increased Glioblastoma Multiforme Growth and Chemoresistance Through LRP6.

Dong-Mei Li, Qiu-Dan Chen, Gui-Ning Wei, Jie Wei, Jian-Xing Yin, Jun-Hui He, Xin Ge, Zhu-Mei Shi

Open access · goldAbstract read
In one paragraph

Article in Frontiers in oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 11% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

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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

8 authors at 4 institutions in 1 country.

Dong-Mei LiDepartment of Pharmacology, Guangxi Institute of Chinese Medicine & Pharmaceutical Science, Nanning, China.
Qiu-Dan ChenThe Department of Central Laboratory, Clinical Laboratory, Jing'an District Center Hospital of Shanghai, Fudan University, Shanghai, China.
Gui-Ning WeiDepartment of Pharmacology, Guangxi Institute of Chinese Medicine & Pharmaceutical Science, Nanning, China.
Jie WeiDepartment of Pharmacology, Guangxi Institute of Chinese Medicine & Pharmaceutical Science, Nanning, China.
Jian-Xing YinInstitute for Brain Tumors, Jiangsu Key Lab of Cancer Biomarkers, Prevention and Treatment, Jiangsu Collaborative Innovation Center for Cancer Personalized Medicine, Nanjing Medical University, Nanjing, China.
Jun-Hui HeDepartment of Pharmacology, Guangxi Institute of Chinese Medicine & Pharmaceutical Science, Nanning, China.
Xin GeInstitute for Brain Tumors, Jiangsu Key Lab of Cancer Biomarkers, Prevention and Treatment, Jiangsu Collaborative Innovation Center for Cancer Personalized Medicine, Nanjing Medical University, Nanjing, China.
Zhu-Mei ShiInstitute for Brain Tumors, Jiangsu Key Lab of Cancer Biomarkers, Prevention and Treatment, Jiangsu Collaborative Innovation Center for Cancer Personalized Medicine, Nanjing Medical University, Nanjing, China.
Guangxi University of Chinese Medicine · CNNanjing Medical University · CNJiangsu Cancer Hospital · CNJinshan Hospital of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeGlioblastoma multiforme (GBM) is one of the deadliest tumors, which is involved in numerous dysregulated microRNAs including miR-137. However, the mechanism of how miR-137 suppression associated with cancer progression and chemoresistance still remains to be elucidated.

methodsQuantitative reverse transcriptase-PCR (qRT-PCR), DNA methylation analysis, cell proliferation assay, flow cytometric analysis, invasion assay,

resultsWe found that miR-137 was downregulated in primary and recurrent GBM compared with normal brain tissues. Overexpression of miR-137 inhibited cell invasion and enhanced cell chemosensitivity to temozolomide (TMZ) by directly targeting low-density lipoprotein receptor-related protein 6 (LRP6) in GBM. Forced expression of LRP6 cDNA without its 3'-UTR region partly restored the effects of miR-137

conclusionsThese findings demonstrated the detailed molecular mechanism of miR-137 in regulating GBM growth and chemoresistance in hypoxia microenvironment, suggesting the potentiality of miR-137 as a therapeutic target for GBM.

Indexed as

chemoresistanceepithelial-mesenchymal transition-related genesglioblastoma multiformeLRP6miR-137

Identifiers

PMID33718112
PMCPMC7946983
OpenAlexW3130927750

What OpenQuestion holds

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LicenceCC BY
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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.