Evidence map›Paper›PMID 29749535›Full record

ArticleOncology reports2018

Oncogenic role of miR‑183‑5p in lung adenocarcinoma: A comprehensive study of qPCR, in vitro experiments and bioinformatic analysis.

Rong-Quan He, Li Gao, Jie Ma, Zu-Yun Li, Xiao-Hua Hu, Gang Chen

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

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  5. APE1 controls DICER1 expression in NSCLC through miR-33a and miR-130b.Cellular and molecular life sciences : CMLS · 2022
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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 2 institutions in 1 country.

Rong-Quan HeDepartment of Medical Oncology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region 530022, P.R. China.
Li GaoDepartment of Pathology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region 530022, P.R. China.
Jie MaDepartment of Medical Oncology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region 530022, P.R. China.
Zu-Yun LiDepartment of Pathology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region 530022, P.R. China.
Xiao-Hua HuDepartment of Medical Oncology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region 530022, P.R. China.
Gang ChenDepartment of Pathology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region 530022, P.R. China.
First Affiliated Hospital of GuangXi Medical University · CNGuangxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite the fact that previous studies have reported the aberrant expression of miR‑183‑5p in lung adenocarcinoma (LUAD), the oncogenic role of miR‑183‑5p in LUAD and its underlying mechanisms have remained elusive. Hence, we attempted to elucidate the clinicopathological significance of miR‑183‑5p expression in LUAD and identify the biological function of miR‑183‑5p in LUAD in this study. Meta‑analysis of Gene Expression Omnibus (GEO) data, data mining of The Cancer Genome Atlas (TCGA) and real‑time quantitative polymerase chain reaction (qPCR) were performed to evaluate the clinicopathological significance of miR‑183‑5p in LUAD. Then, the effect of miR‑183‑5p on cell growth in LUAD was assessed by in vitro experiments. Additionally, the target genes of miR‑183‑5p were identified via miRWalk v.2.0 and TCGA. Gene Ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis and Disease Ontology (DO) analysis were further carried out for the target genes. The targetability between target genes in key KEGG pathways and miR‑183‑5p was validated by independent samples t‑test, Pearson's correlation test and immunohistochemistry results from the Human Protein Atlas (HPA). According to the results, miR‑183‑5p was overexpressed in LUAD and exhibited significant diagnostic value. Moreover, miR‑183 expression was associated with tumor progression in the TCGA data. In vitro experiments revealed the positive influence of miR‑183‑5p on cell viability and proliferation as well as the negative effect of miR‑183‑5p on caspase‑3/7 activity in LUAD, which supports the finding that target genes of miR‑183‑5p are mainly enriched in gene pathways containing cell adhesion molecules (CAMs) and gene pathways important in cancer. Therefore, we conclude that miR‑183‑5p acts as an oncogene in LUAD and participates in the pathogenesis of LUAD via the interaction networks of its target genes.

Indexed as

AdenocarcinomaAdenocarcinoma of LungBiomarkers, TumorCarcinogenesisCell Line, TumorCell ProliferationComputational BiologyGene Expression Regulation, NeoplasticHumansLung NeoplasmsMicroRNAsOncogenesBiomarkers, TumorMicroRNAsMIRN183 microRNA, human

Identifiers

PMID29749535
PMCPMC6059757
OpenAlexW2801631322

What OpenQuestion holds

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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.