Evidence map›Paper›PMID 30320391›Full record

SynthesisMolecular medicine reports2018

Upregulated miR‑203a‑3p and its potential molecular mechanism in breast cancer: A study based on bioinformatics analyses and a comprehensive meta‑analysis.

Kai-Teng Cai, Cai-Xia Feng, Jin-Che Zhao, Rong-Quan He, Jie Ma, Jin-Cai Zhong

Open access · hybridAbstract readMeta-Analysis
In one paragraph

Synthesis in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 2 pooled it
0.7field-weighted citation impact, top 35% 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, 2 syntheses or guidelines pooled it, 24 citations in OpenAlex.

  1. Pooled it
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  11. miR-205-5p Downregulation andInternational journal of molecular sciences · 2021
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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.

Kai-Teng CaiDepartment of Medical Oncology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region 530021, P.R. China.
Cai-Xia FengDepartment of Medical Oncology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region 530021, P.R. China.
Jin-Che ZhaoDepartment of Medical Oncology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region 530021, P.R. China.
Rong-Quan HeDepartment of Medical Oncology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region 530021, P.R. China.
Jie MaDepartment of Medical Oncology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region 530021, P.R. China.
Jin-Cai ZhongDepartment of Medical Oncology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region 530021, 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

Breast cancer (BC) has been identified as the leading malignancy in women worldwide. However, the potential molecular mechanism of microRNA (miR)‑203a‑3p in BC remains to be elucidated. The present study evaluated the expression of miR‑203a‑3p in BC and adjacent normal tissue in several publically available datasets. The distinguishability of precursor miR‑203a and miR‑203a‑3p in BC tissue and adjacent breast tissue was assessed using receiver operating characteristic (ROC) and summarized ROC (sROC) approaches. In addition, gene ontology (GO) enrichment, Kyoto Encyclopedia of Genes and Genomes pathway analysis and protein‑protein interaction analysis were performed to determine the potential molecular mechanism of miR‑203a‑3p in BC. It was identified that the expression of precursor miR‑203a was markedly upregulated in 1,077 BC tissue samples compared to 104 adjacent breast tissue samples from The Cancer Genome Atlas. Additionally, an increasing trend in miR‑203a‑3p expression was observed in 756 BC tissue samples compared with 76 adjacent breast tissue samples from the University of California Santa Cruz Xena project. In addition, a comprehensive meta‑analysis suggested that the expression of miR‑203a‑3p was markedly increased in 2,444 BC tissue samples compared with 559 adjacent breast tissue samples. The area under the curve of the ROC and sROC revealed that miR‑203a‑3p expression was able to distinguish between BC tissue and adjacent breast tissue. However, miR‑203a‑3p exhibited no prognostic value in BC. The results of GO enrichment demonstrated that the miR‑203a target genes were associated with 'plasma membrane integrity', 'cell surface receptor linked signal and transduction' and '3',5'‑cyclic nucleotide phosphodiesterase activity'. 'Purine metabolism' was identified as the pathway with the most enrichment of miR‑203a‑3p target genes in BC. The present study also identified insulin‑like growth factor receptor (IGF1) as a hub gene associated with miR‑203a in BC. In summary, miR‑203a‑3p may enhance the development and oncogenesis of BC, and IGF1 was defined as a hub gene of miR‑203a‑3p in BC.

Indexed as

Gene Expression Regulation, NeoplasticAdultAgedBiomarkers, TumorBreast NeoplasmsComputational BiologyFemaleGene Expression ProfilingGene OntologyHumansMicroRNAsMiddle AgedNeoplasm StagingPrognosisProtein Interaction MappingProtein Interaction MapsBiomarkers, TumorMicroRNAsMIRN203 microRNA, humanbreast cancergene expression omnibusmicroRNA‑203a‑3ptarget genethe cancer genome atlas

Identifiers

PMID30320391
PMCPMC6236224
OpenAlexW2896010468

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.