PMID- 29257263
OWN - NLM
STAT- MEDLINE
DCOM- 20180803
LR  - 20180803
IS  - 1791-3004 (Electronic)
IS  - 1791-2997 (Linking)
VI  - 17
IP  - 2
DP  - 2018 Feb
TI  - miR‑137 decreases proliferation, migration and invasion in rheumatoid arthritis 
      fibroblast‑like synoviocytes.
PG  - 3312-3317
LID - 10.3892/mmr.2017.8225 [doi]
AB  - MicroRNA-137 (miR-137) is involved in cell proliferation, migration, invasion and 
      apoptosis in a variety of cells. However, the role of miR‑137 in rheumatoid 
      arthritis (RA) remains unclear. The present study aimed to identify the 
      biological roles of miR‑137 in RA. The expression of miR‑137 in RA 
      fibroblast‑like synoviocytes (RA‑FLS) and in normal control FLS was detected by 
      reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR). The 
      effects of miR‑137 on RA‑FLS proliferation, migration and invasion were also 
      determined using MTT, wound healing and Transwell invasion assays, respectively. 
      The effects of miR‑137 on inflammatory cytokine expression in RA‑FLS were 
      assessed by ELISA. Bioinformatics databases (TargetScan and miRanda), luciferase 
      reporter assays, RT‑qPCR and western blotting assays were conducted to identify 
      potential target genes. miR‑137 expression was decreased in RA‑FLS compared with 
      expression in normal control FLS. Overexpression of miR‑137 resulted in a 
      significant reduction in RA‑FLS proliferation, migration and invasion, and 
      decreased the expression of inflammatory cytokines of RA‑FLS. In addition, 
      bioinformatics analysis and luciferase reporter assays indicated that miR‑137 may 
      target the 3'‑untranslated region of C‑X‑C motif chemokine ligand 12 (CXCL12), 
      which was confirmed by RT‑qPCR and western blot analyses. These results further 
      demonstrated that miR‑137may serve an inhibitory role in RA by targeting CXCL12 
      expression, and miR‑137 may be a potential target for the treatment of RA.
FAU - Du, Juan
AU  - Du J
AD  - Department of Rheumatology and Immunology, China‑Japan Union Hospital of Jilin 
      University, Changchun, Jilin 130033, P.R. China.
FAU - Zhang, Fangze
AU  - Zhang F
AD  - Endoscope Center, China‑Japan Union Hospital of Jilin University, Changchun, 
      Jilin 130033, P.R. China.
FAU - Guo, Jialong
AU  - Guo J
AD  - Department of Rheumatology and Immunology, China‑Japan Union Hospital of Jilin 
      University, Changchun, Jilin 130033, P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20171208
PL  - Greece
TA  - Mol Med Rep
JT  - Molecular medicine reports
JID - 101475259
RN  - 0 (MIRN137 microRNA, rat)
RN  - 0 (MicroRNAs)
SB  - IM
MH  - Animals
MH  - Arthritis, Rheumatoid/*genetics/pathology
MH  - Cell Movement
MH  - Cell Proliferation
MH  - Cells, Cultured
MH  - Disease Progression
MH  - Fibroblasts/metabolism/*pathology
MH  - Male
MH  - MicroRNAs/*genetics
MH  - Rats, Wistar
MH  - Synoviocytes/metabolism/*pathology
MH  - *Up-Regulation
EDAT- 2017/12/20 06:00
MHDA- 2018/08/04 06:00
CRDT- 2017/12/20 06:00
PHST- 2016/08/02 00:00 [received]
PHST- 2017/05/05 00:00 [accepted]
PHST- 2017/12/20 06:00 [pubmed]
PHST- 2018/08/04 06:00 [medline]
PHST- 2017/12/20 06:00 [entrez]
AID - 10.3892/mmr.2017.8225 [doi]
PST - ppublish
SO  - Mol Med Rep. 2018 Feb;17(2):3312-3317. doi: 10.3892/mmr.2017.8225. Epub 2017 Dec 
      8.