PMID- 35164656
OWN - NLM
STAT- MEDLINE
DCOM- 20220408
LR  - 20220712
IS  - 2165-5987 (Electronic)
IS  - 2165-5979 (Print)
IS  - 2165-5979 (Linking)
VI  - 13
IP  - 3
DP  - 2022 Mar
TI  - LncRNA OSER1-AS1 regulates the inflammation and apoptosis of rheumatoid arthritis 
      fibroblast like synoviocytes via regulating miR-1298-5p/E2F1 axis.
PG  - 4951-4963
LID - 10.1080/21655979.2022.2037854 [doi]
AB  - It has been reported that long noncoding RNAs (LncRNAs) take part in the 
      progression and occurrence of rheumatoid arthritis (RA). The current work aimed 
      to dig the effect of lncRNA OSER1-AS1 on RA and the associated mechanism. 
      Quantitative real-time polymerase chain reaction (qRT-PCR) was made to decide 
      that OSER1-AS1 was significantly lowly expressed in synovial tissue and serum of 
      RA patients, which was consistent in RA-FLSs cell lines. The result of ROC curve 
      indicated that OSER1-AS1 could be a diagnostic biomarker for RA patients. Cell 
      Counting Kit-8 assay (CCK-8), EdU staining and flow cytometry were performed to 
      explore the effect of OSER1-AS1 on RA-FLSs in vitro. Relative levels of 
      interleukin-1 (IL-1), interleukin-6 (IL-6), matrix metalloproteinases-3 (MMP-3) 
      were detected by ELISA and the result displayed that overexpression of OSER1-AS1 
      inhibited RA-induced inflammatory production of IL-1, IL-6 and MMP3. 
      Bioinformatics analysis, luciferase reporter, RNA immunoprecipitation assays 
      (RIP) and RNA pull-down assay were conducted to confirm the binding between 
      microRNA-1298-5p (miR-1298-5p) and OSER1-AS1 or E2F transcription factor 1 
      (E2F1). Mechanistically, OSER1-AS1 serves as a competing endogenous (ceRNA) in 
      RA-FLSs through the sponge of miR-1298-5p and increase in the expression of E2F1. 
      Further restoration experiments revealed that miR-1298-5p mimics and E2F1 
      silencing could partially reverse the inhibiting effect of OSER1-AS1 
      overexpression on propagation and apoptosis in RA-FLSs. The results illustrated 
      the biological mechanism of OSER1-AS1/miR-1298-59/E2F1 axis in RA progression. 
      The outcomes indicated that OSER1-AS1 might be adopted as a hopeful diagnostic 
      and therapeutic objective for RA.
FAU - Fu, Qiang
AU  - Fu Q
AD  - Department of Rheumatology and Immunology, Jiangxi Provincial People's Hospital 
      Affiliated to Nanchang University, Nanchang, Jiangxi, China.
FAU - Song, Mei-Jie
AU  - Song MJ
AD  - Department of Rheumatology and Immunology, Jiangxi Provincial People's Hospital 
      Affiliated to Nanchang University, Nanchang, Jiangxi, China.
FAU - Fang, Jing
AU  - Fang J
AD  - Geriatric Department, Jiangxi Provincial People's Hospital Affiliated to Nanchang 
      University, Nanchang, Jiangxi, China.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Bioengineered
JT  - Bioengineered
JID - 101581063
RN  - 0 (E2F1 Transcription Factor)
RN  - 0 (E2F1 protein, human)
RN  - 0 (Interleukin-1)
RN  - 0 (Interleukin-6)
RN  - 0 (MIRN1298 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - 0 (RNA, Long Noncoding)
SB  - IM
MH  - Apoptosis/genetics
MH  - *Arthritis, Rheumatoid/genetics/metabolism
MH  - Cell Proliferation/genetics
MH  - *E2F1 Transcription Factor/metabolism
MH  - Fibroblasts/metabolism
MH  - Humans
MH  - Inflammation/genetics/metabolism
MH  - Interleukin-1/metabolism
MH  - Interleukin-6/genetics/metabolism
MH  - *MicroRNAs/genetics/metabolism
MH  - *RNA, Long Noncoding/genetics/metabolism
MH  - *Synoviocytes/metabolism
PMC - PMC8974142
OTO - NOTNLM
OT  - E2F1
OT  - OSER1-AS1
OT  - miR-1298-5p
OT  - rheumatoid arthritis
COIS- No potential conflict of interest was reported by the author(s).
EDAT- 2022/02/16 06:00
MHDA- 2022/04/09 06:00
PMCR- 2022/02/14
CRDT- 2022/02/15 05:30
PHST- 2022/02/15 05:30 [entrez]
PHST- 2022/02/16 06:00 [pubmed]
PHST- 2022/04/09 06:00 [medline]
PHST- 2022/02/14 00:00 [pmc-release]
AID - 2037854 [pii]
AID - 10.1080/21655979.2022.2037854 [doi]
PST - ppublish
SO  - Bioengineered. 2022 Mar;13(3):4951-4963. doi: 10.1080/21655979.2022.2037854.