Evidence map›Paper›PMID 32199129›Full record

ArticleMolecular therapy. Nucleic acids2020

Silencing lncRNA AGAP2-AS1 Upregulates miR-195-5p to Repress Migration and Invasion of EC Cells via the Decrease of FOSL1 Expression.

Sining Shen, Ke Li, Ying Liu, Xianben Liu, Baoxing Liu, Yufeng Ba, Wenqun Xing

Open access · goldAbstract read
In one paragraph

Article in Molecular therapy. Nucleic acids, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.9field-weighted citation impact, top 3% 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

33 citing papers in PubMed, 81 citations in OpenAlex.

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  9. Long Non-Coding RNAMolecules (Basel, Switzerland) · 2024
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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

7 authors at 1 institution in 1 country.

Sining ShenDepartment of Thoracic Surgery, Affiliated Cancer Hospital of Zhengzhou University (Henan Cancer Hospital), Zhengzhou 450008, P.R. China. Electronic address: shen_sining@163.com.
Ke LiDepartment of Oncology, Affiliated Cancer Hospital of Zhengzhou University (Henan Cancer Hospital), Zhengzhou 450008, P.R. China.
Ying LiuDepartment of Oncology, Affiliated Cancer Hospital of Zhengzhou University (Henan Cancer Hospital), Zhengzhou 450008, P.R. China.
Xianben LiuDepartment of Thoracic Surgery, Affiliated Cancer Hospital of Zhengzhou University (Henan Cancer Hospital), Zhengzhou 450008, P.R. China.
Baoxing LiuDepartment of Thoracic Surgery, Affiliated Cancer Hospital of Zhengzhou University (Henan Cancer Hospital), Zhengzhou 450008, P.R. China.
Yufeng BaDepartment of Thoracic Surgery, Affiliated Cancer Hospital of Zhengzhou University (Henan Cancer Hospital), Zhengzhou 450008, P.R. China.
Wenqun XingDepartment of Thoracic Surgery, Affiliated Cancer Hospital of Zhengzhou University (Henan Cancer Hospital), Zhengzhou 450008, P.R. China.
Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The interaction of long non-coding RNAs (lncRNAs), microRNAs (miRNAs), and mRNAs has been implicated in various types of cancers, including esophageal cancer (EC). The current study aimed to investigate the role of AGAP2-AS1/miR-195-5p/Fos-like antigen-1 (FOSL1) in EC progression. The expression of AGAP2-AS1, miR-195-5p, and FOSL1 in tumor tissues isolated from EC patients and EC cell lines was determined by quantitative reverse transcriptase polymerase chain reaction (qRT-PCR), the results of which illustrated that AGAP2-AS1 and FOSL1 were increased while miR-195-5p was reduced in EC. Next, the ectopic expression, knockdown, and reporter assay experiments were all employed to elucidate the mechanism of AGAP2-AS1/miR-195-5p/FOSL1 in the processes of EC cell proliferation, cell cycle, apoptosis, invasion, and migration as well as tumor growth. Knockdown of AGAP2-AS1 or overexpression of miR-195-5p reduced EC cell proliferation, migration, and invasion, blocked cell cycle entry, and elevated apoptosis. FOSL1 was found to be specifically targeted by miR-195-5p. AGAP2-AS1 was observed to upregulate FOSL1 by binding to miR-195-5p. Silencing of AGAP2-AS1 was observed to restrain the development of EC both in vitro and in vivo through upregulating miR-195-5p and downregulating FOSL1. Taken together, AGAP2-AS1 knockdown exercises suppressive effects on the development of EC through miR-195-5p-dependent downregulation of FOSL1. Therefore, targeting AGAP2-AS1 could be a future direction to develop a novel molecule-targeted therapeutic strategy for EC.

Indexed as

apoptosisesophageal cancerFOSL1invasionlong non-coding AGAP2-AS1microRNA-195-5pmigrationproliferation

Identifiers

PMID32199129
PMCPMC7082499
OpenAlexW2998905211

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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.