Evidence map›Paper›PMID 28416776›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2017

Clinical Value of miR-101-3p and Biological Analysis of its Prospective Targets in Breast Cancer: A Study Based on The Cancer Genome Atlas (TCGA) and Bioinformatics.

Chun-Yao Li, Dan-Dan Xiong, Chun-Qin Huang, Rong-Quan He, Hai-Wei Liang, Deng-Hua Pan, Han-Lin Wang, Yi-Wen Wang, Hua-Wei Zhu, Gang Chen

Open access · hybridAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed, 29 citations in OpenAlex.

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  17. High expression of SLC6A10P contributes to poor prognosis in lung adenocarcinoma.International journal of clinical and experimental pathology · 2018
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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

10 authors at 2 institutions in 1 country.

Chun-Yao LiDepartment of Pathology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China (mainland).
Dan-Dan XiongDepartment of Pathology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China (mainland).
Chun-Qin HuangDepartment of Pathology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China (mainland).
Rong-Quan HeDepartment of Medical Oncology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China (mainland).
Hai-Wei LiangDepartment of Pathology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China (mainland).
Deng-Hua PanDepartment of Medical Ultrasonics, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China (mainland).
Han-Lin WangDepartment of Pathology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China (mainland).
Yi-Wen WangDepartment of Pathology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China (mainland).
Hua-Wei ZhuDepartment of Medical Oncology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China (mainland).
Gang ChenDepartment of Pathology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China (mainland).
Guangxi Medical University · CNFirst Affiliated Hospital of GuangXi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND MiR-101-3p can promote apoptosis and inhibit proliferation, invasion, and metastasis in breast cancer (BC) cells. However, its mechanisms in BC are not fully understood. Therefore, a comprehensive analysis of the target genes, pathways, and networks of miR-101-3p in BC is necessary. MATERIAL AND METHODS The miR-101 profiles for 781 patients with BC from The Cancer Genome Atlas (TCGA) were analyzed. Gene expression profiling of GSE31397 with miR-101-3p transfected MCF-7 cells and scramble control cells was downloaded from Gene Expression Omnibus (GEO), and the differentially expressed genes (DEGs) were identified. The potential genes targeted by miR-101-3p were also predicted. Gene Ontology (GO) and pathway and network analyses were constructed for the DEGs and predicted genes. RESULTS In the TCGA data, a low level of miR-101-2 expression might represent a diagnostic (AUC: 0.63) marker, and the miR-101-1 was a prognostic (HR=1.79) marker. MiR-101-1 was linked to the estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2), and miR-101-2 was associated with the tumor (T), lymph node (N), and metastasis (M) stages of BC. Moreover, 427 genes were selected from the 921 DEGs in GEO and the 7924 potential target genes from the prediction databases. These genes were related to transcription, metabolism, biosynthesis, and proliferation. The results were also significantly enriched in the VEGF, mTOR, focal adhesion, Wnt, and chemokine signaling pathways. CONCLUSIONS MiR-101-1 and miR-101-2 may be prospective biomarkers for the prognosis and diagnosis of BC, respectively, and are associated with diverse clinical parameters. The target genes of miR-101-3p regulate the development and progression of BC. These results provide insight into the pathogenic mechanism and potential therapies for BC.

Indexed as

Biomarkers, TumorBreast NeoplasmsComputational BiologyFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticGene OntologyHumansMCF-7 CellsMicroRNAsPrognosisProspective StudiesReceptors, EstrogenRNA, MessengerBiomarkers, TumorMicroRNAsMIRN101 microRNA, humanReceptors, EstrogenRNA, Messenger

Identifiers

PMID28416776
PMCPMC5404822
OpenAlexW2607134331

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.