Evidence map›Paper›PMID 32494198›Full record

ArticleCancer management and research2020

Upregulation of miR-340 Inhibits Tumor Growth and Mesenchymal Transition via Targeting c-MET in Glioblastoma.

Ning Lin, Wentao Li, Xiefeng Wang, Shiqiang Hou, Dong Yu, Xingyuan Zhao, Chunjing Jin, Guoquan Yao, Wei Yan, Yongping You

Open access · goldAbstract read
In one paragraph

Article in Cancer management and research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 58% 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

1 citing paper in PubMed, 4 citations in OpenAlex.

  1. Article
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 3 institutions in 1 country.

Ning Lin *Department of Neurosurgery, Chuzhou Clinical College of Anhui Medical University, The First People's Hospital Chuzhou, Chuzhou, People's Republic of China.
Wentao Li *Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, People's Republic of China.
Xiefeng Wang *Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, People's Republic of China.
Shiqiang HouDepartment of Neurosurgery, Chuzhou Clinical College of Anhui Medical University, The First People's Hospital Chuzhou, Chuzhou, People's Republic of China.ORCID 0000-0002-5117-7442
Dong YuDepartment of Neurosurgery, Chuzhou Clinical College of Anhui Medical University, The First People's Hospital Chuzhou, Chuzhou, People's Republic of China.
Xingyuan ZhaoDepartment of Neurosurgery, Chuzhou Clinical College of Anhui Medical University, The First People's Hospital Chuzhou, Chuzhou, People's Republic of China.
Chunjing JinLaboratory Medicine Center, Affiliated Hospital of Nantong University, Nantong, People's Republic of China.
Guoquan YaoDepartment of Neurosurgery, Chuzhou Clinical College of Anhui Medical University, The First People's Hospital Chuzhou, Chuzhou, People's Republic of China.
Wei YanDepartment of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, People's Republic of China.
Yongping YouDepartment of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, People's Republic of China.
Anhui Medical University · CNJiangsu Province Hospital · CNNantong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEpithelial-mesenchymal Transition (EMT) is involved in various cancers including glioblastoma. Our previous study has shown that miR-340 negatively correlated with EMT process in glioblastoma. PURPOSE: In the present study, we aim to explore the underlying molecular mechanisms of miR-340 in EMT process of glioblastomas. MATERIALS AND

methodsUsing RT-qPCR assay, we analyzed the expression of miR-340 in glioma cell lines and normal human glia (NHA) cell line. Using CCK8, Colony formation assays, transwell and Western blot assays, we investigated tumor growth and EMT process. Using luciferase reporter assay, we confirmed a target of miR-340.

resultsOur results showed that miR-340 was down-regulated in glioma cell lines (U87, U251 and LN229) compared to NHA cells. MiR-340 overexpression remarkably inhibited cell proliferation and invasion as well as up-regulated E-cadherin expression and down-regulated N-cadherin, Vimentin, ZEB1, Slug and Snail expressions in U251 and LN229 cells. Further studies have confirmed c-MET as a target gene of miR-340. The EMT-inhibitory effect of miR-340 was lost after c-MET expression was restored. We also identified the antitumorigenic activity of miR-340 in vivo.

conclusionThese results demonstrated that miR-340 functioned as a tumor suppressor via targeting EMT process and could be a potential therapeutic candidate for treating glioblastomas.

Indexed as

c-METEMTglioblastomamiR-340

Identifiers

PMID32494198
PMCPMC7229788
OpenAlexW3020818037

What Socratic holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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 Socratic graph.