Evidence map›Paper›PMID 30280514›Full record

ArticleCancer medicine2018

Downregulated miR-144-3p contributes to progression of lung adenocarcinoma through elevating the expression of EZH2.

Chao Liu, Zuozhang Yang, Zhiyong Deng, Youjun Zhou, Quan Gong, Ruilian Zhao, Ting Chen

Open access · goldAbstract read
In one paragraph

Article in Cancer medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.4field-weighted citation impact, top 22% 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

21 citing papers in PubMed, 30 citations in OpenAlex.

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  20. Bioscience reports · 2019
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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.

Chao LiuDepartment of Nuclear Medicine, Tumor Hospital of Yunnan Province, The Third Affiliated Hospital of Kunming Medical College, Kunming, Yunnan, China.
Zuozhang YangDepartments of Orthopaedics, Tumor Hospital of Yunnan Province, The Third Affiliated Hospital of Kunming Medical College, Kunming, Yunnan, China.
Zhiyong DengDepartment of Nuclear Medicine, Tumor Hospital of Yunnan Province, The Third Affiliated Hospital of Kunming Medical College, Kunming, Yunnan, China.
Youjun ZhouDepartment of Nuclear Medicine, The Affiliated Yan'an Hospital of Kunming Medical College, Kunming, Yunnan, China.
Quan GongDepartment of Palliative Medicine, Tumor Hospital of Yunnan Province, The Third Affiliated Hospital of Kunming Medical College, Kunming, Yunnan, China.
Ruilian ZhaoDepartments of Combination of Chinese Traditional and Western Medicine, Tumor Hospital of Yunnan Province, The Third Affiliated Hospital of Kunming Medical College, Kunming, Yunnan, China.
Ting ChenDepartment of Nuclear Medicine, Tumor Hospital of Yunnan Province, The Third Affiliated Hospital of Kunming Medical College, Kunming, Yunnan, China.ORCID 0000-0002-1984-3003
Kunming Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesThe intention of our study was to investigate the relationship between miR-144-3p and EZH2 as well as the effects of their interaction on cell propagation and invasiveness in lung adenocarcinoma (LUAD).

methodsThe expression levels of miR-144-3p and EZH2 in LUAD tissues and normal tissues were determined by qRT-PCR. The dual-luciferase reporter assay was utilized to validate the targeting relationship between miR-144-3p and EZH2. MTT assay and colony formation assay were performed to evaluate the viability and propagation of LUAD cells, while the effects of miR-144-3p and EZH2 on LUAD cell invasiveness were confirmed by transwell assay. Protein expression levels of VEGFA, MMP2, and MMP9 were measured by Western blot. Furthermore, xenograft tumor models were established to verify the effects of miR-144-3p on tumor formation and EZH2, VEGFA, MMP2 and MMP9 expressions in vivo.

resultsmiR-144-3P was downregulated in LUAD tissues, and overexpression of miR-144-3p inhibited propagation and invasiveness of LUAD cells. EZH2 was a target of miR-144-3p and was highly expressed in LUAD cells. Knockdown of EZH2 could suppress the propagation and invasion of LUAD cells. Increased miR-144-3p expression exerted an inhibitory effect on LUAD tumor formation in vivo.

conclusionOverexpression of miR-144-3p impeded the propagation and invasiveness of LUAD cells by targeting EZH2.

Indexed as

Down-RegulationAdenocarcinoma of LungAnimalsCell Line, TumorDisease ProgressionEnhancer of Zeste Homolog 2 ProteinFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansLung NeoplasmsMaleMiceMicroRNAsNeoplasm InvasivenessNeoplasm TransplantationEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanMicroRNAsMIRN144 microRNA, humanEZH2lung adenocarcinomamiR-144-3p

Identifiers

PMID30280514
PMCPMC6246953
OpenAlexW2894860758

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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.