Evidence map›Paper›PMID 31168689›Full record

ArticleHuman cell2019

MiR-142-3p suppresses the proliferation, migration and invasion through inhibition of NR2F6 in lung adenocarcinoma.

Chang'e Jin, Liang Xiao, Zeqiang Zhou, Yan Zhu, Geng Tian, Shuhua Ren

Abstract read
PubMed Publisher
In one paragraph

Article in Human cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

25 citing papers in PubMed, 78 citations in OpenAlex.

  1. Review
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  7. Regulatory role of the miR-142-3p/Translational lung cancer research · 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

6 authors at 3 institutions in 1 country.

Chang'e Jin *Department of Respiratory and Critical Care Medicine, Shenzhen People's Hospital, Second Clinical Medical College of Jinan University, Shenzhen, 518020, Guangdong, China.
Liang Xiao *Department of Surgery and Oncology, Shenzhen Second People's Hospital, First Affiliated Hospital to Shenzhen University, Shenzhen, 518035, Guangdong, China.
Zeqiang Zhou *Department of Surgery and Oncology, Shenzhen Second People's Hospital, First Affiliated Hospital to Shenzhen University, Shenzhen, 518035, Guangdong, China.
Yan ZhuDepartment of Surgery and Oncology, Shenzhen Second People's Hospital, First Affiliated Hospital to Shenzhen University, Shenzhen, 518035, Guangdong, China.
Geng TianDepartment of Surgery and Oncology, Shenzhen Second People's Hospital, First Affiliated Hospital to Shenzhen University, Shenzhen, 518035, Guangdong, China.
Shuhua RenDepartment of Thoracic Surgery, Tangshan Gongren Hospital, No. 27, Wenhua Road, Tangshan, 063000, Hebei, China. renshuhua2018@sohu.com.
Shenzhen Second People's Hospital · CNJinan University · CNTangshan Gongren Hospital · CN

Funding

Sanming Project of Shenzhen Health and Family Planning Commission SZSM201512016
6 · The paper itself

Abstract

Non-small cell lung cancer (NSCLC) is the leading cause of cancer-related death worldwide and lung adenocarcinoma is its main type. MicroRNAs are small, non-coding and single-strand RNAs that regulate gene expression in human cancers. The aim of our study is to investigate the underlying molecular mechanism of miR-142-3p in NSCLC. The expression of miR-142-3p in lung adenocarcinoma tissues and cells was detected by RT-qPCR. Next, cell proliferation, migration, invasion and apoptosis were examined by CCK-8, scratch assay, transwell assay and flow cytometry in A549 and HCC827 cells, respectively. Then, the target of miR-142-3p was predicted by targetscanHuman 7.2 and confirmed using dual-luciferase reporter assay. Additionally, RT-qPCR and western blot were used to detect the expression of NR2F6, MMP2, MMP9 and caspase-3. The results showed that miR-142-3p expression was significantly decreased in tumor tissues and cells. Overexpression of miR-142-3p inhibited the proliferation, migration, invasion and promoted cell apoptosis in vitro, while knockdown of miR-142-3p had reversed function. Furthermore, NR2F6 was identified as a direct target of miR-142-3p, which was negatively correlated with miR-142-3p expression. Finally, miR-142-3p overexpression suppressed the expression of NR2F6, MMP2 and MMP9, but improved caspase-3 expression, while miR-142-3p knockdown got the opposite expression results. Suppressing MMP2 and MMP9 activities inhibited cell invasion. In summary, these findings indicated that miR-142-3p inhibits lung adenocarcinoma cell proliferation, migration and invasion, and enhances cell apoptosis by targeting NR2F6, suggesting that miR-142-3p may be a novel therapeutic target for lung adenocarcinoma treatment.

Indexed as

AdenocarcinomaAdultAgedApoptosisCell MovementCell ProliferationFemaleGene ExpressionGene Expression Regulation, NeoplasticHumansLung NeoplasmsMaleMicroRNAsMiddle AgedMolecular Targeted TherapyNeoplasm InvasivenessMicroRNAsMIRN142 microRNA, humanNR2F6 protein, humanRepressor ProteinsInvasionLung adenocarcinomaMigrationMiR-142-3pNR2F6

Identifiers

PMID31168689
OpenAlexW2965405909

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.