PMID- 30655760
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200930
IS  - 1792-1074 (Print)
IS  - 1792-1082 (Electronic)
IS  - 1792-1074 (Linking)
VI  - 17
IP  - 1
DP  - 2019 Jan
TI  - Investigation of the clinical significance and molecular mechanism of miR-21-5p 
      in hepatocellular carcinoma: A systematic review based on 24 studies and 
      bioinformatics investigation.
PG  - 230-246
LID - 10.3892/ol.2018.9627 [doi]
AB  - To investigate the prospective roles and the clinicopathological application of 
      microRNA-21-5p (miR-21-5p) in hepatocellular carcinoma (HCC), the present review 
      is based on 24 studies and bioinformatics investigation. Firstly, HCC-associated 
      miR-21-5p data were aggregated from literature databases and two public genomic 
      data repositories, including the Gene Expression Omnibus (GEO) and The Cancer 
      Genome Atlas (TCGA). Potential target genes of miR-21-5p in HCC were identified 
      using TCGA and GEO, Natural Language Processing and 14 online software packages. 
      The oncogenic roles of these target genes was probed for understanding using 
      Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) analysis. 
      Hub genes were further investigated by protein-protein interaction network (PPI) 
      analysis. Comprehensive meta-analysis, including 10 microarrays from GEO 
      datasets, 13 literature studies and TCGA-based RNA sequencing data, indicated a 
      reliable diagnostic capacity of miR-21-5p [area under the curve (AUC), 0.887; 
      sensitivity, 0.78% and specificity, 0.79%]. The healthy control group (AUC, 
      0.926; sensitivity, 0.87% and specificity, 0.82%) demonstrated high diagnostic 
      capacity of miR-21-5p compared with the chronic hepatitis B infection group (AUC, 
      0.904; sensitivity, 0.75% and specificity, 0.84%). A total of 10 significant 
      enrichment pathways were indicated by KEGG analysis, with cytokine-cytokine 
      receptor interaction exhibiting the highest score. A total of 5 genes, hepatocyte 
      growth factor, forkhead box O1 (FOXO1), thrombospondin 1, estrogen receptor 1 
      (ESR1) and C-X-C motif chemokine ligand 12 were selected from 39 overlapping 
      genes, according to the PPI network. Target genes were assembled in GO terms 
      associated with 'response to chemical stimulus', 'cell surface' and 'growth 
      factor binding'. In particular, low expression of FOXO1 and ESR1 was associated 
      with miR-21-5p expression. In conclusion, upregulated expression of miR-21-5p may 
      be a functional regulator of the metabolism or apoptosis in HCC and a novel tumor 
      marker for the early diagnosis of HCC.
FAU - Zhong, Xiao-Zhu
AU  - Zhong XZ
AD  - Department of Medical Ultrasonics, The First Affiliated Hospital of Guangxi 
      Medical University, Nanning, Guangxi Zhuang Autonomous Region 530021, P.R. China.
FAU - Deng, Yun
AU  - Deng Y
AD  - Department of Pathology, The First Affiliated Hospital of Guangxi Medical 
      University, Nanning, Guangxi Zhuang Autonomous Region 530021, P.R. China.
FAU - Chen, Gang
AU  - Chen G
AD  - Department of Pathology, The First Affiliated Hospital of Guangxi Medical 
      University, Nanning, Guangxi Zhuang Autonomous Region 530021, P.R. China.
FAU - Yang, Hong
AU  - Yang H
AD  - Department of Medical Ultrasonics, The First Affiliated Hospital of Guangxi 
      Medical University, Nanning, Guangxi Zhuang Autonomous Region 530021, P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20181026
PL  - Greece
TA  - Oncol Lett
JT  - Oncology letters
JID - 101531236
PMC - PMC6313181
OTO - NOTNLM
OT  - bioinformatics enrichment analysis
OT  - diagnostic value
OT  - hepatocellular carcinoma
OT  - miR-21-5p
OT  - target genes
EDAT- 2019/01/19 06:00
MHDA- 2019/01/19 06:01
PMCR- 2018/10/26
CRDT- 2019/01/19 06:00
PHST- 2017/11/27 00:00 [received]
PHST- 2018/06/26 00:00 [accepted]
PHST- 2019/01/19 06:00 [entrez]
PHST- 2019/01/19 06:00 [pubmed]
PHST- 2019/01/19 06:01 [medline]
PHST- 2018/10/26 00:00 [pmc-release]
AID - OL-0-0-9627 [pii]
AID - 10.3892/ol.2018.9627 [doi]
PST - ppublish
SO  - Oncol Lett. 2019 Jan;17(1):230-246. doi: 10.3892/ol.2018.9627. Epub 2018 Oct 26.