Table2_Long Non-Coding RNA NR-133666 Promotes the Proliferation and Migration of Fibroblast-Like Synoviocytes Through Regulating the miR-133c/MAPK1 Axis.DOCX
Long non-coding RNA (lncRNA) is involved in the regulation of rheumatoid arthritis (RA) and many other diseases. In this study, a new lncRNA, NR-133666, was identified to be highly expressed in the adjuvant-induced arthritis rat model using the Agilent lncRNA microarray assay. qRT-PCR verified that NR-133666 was upregulated in fibroblast-like synoviocyte of a collagen-induced arthritis (CIA) rat model. Fluorescence in situ hybridization analysis showed that NR-133666 is mainly expressed in the cytoplasm of collagen-induced arthritis FLS. MTT assay and EdU staining results showed that the proliferation of CIA FLS was inhibited after NR-133666 was knocked down, and the wound healing assay showed that the migration of CIA FLS was also suppressed. Dual luciferase detection was used to confirm the relationship among NR-133666, miR-133c and MAPK1. MAPK1 is the target gene of miR-133c, where NR-133666 acts as a sponge of miR-133c to reduce the inhibitory effect of miR-133c on MAPK1. Overexpression of NR-133666 and MAPK1 can promote the proliferation and migration of CIA FLS, and overexpression of miR-133c can reverse this phenomenon. Western blot indicated that it may be related to the ERK/MAPK signaling pathway. Collectively, we identified that lncRNA NR-133666 acted as a miR-133c sponge that can promote the proliferation and migration of CIA FLS through regulating the miR-133c/MAPK1 axis.
History
References
- https://doi.org//10.1002/cam4.2675
- https://doi.org//10.1038/nrrheum.2012.190
- https://doi.org//10.3389/fimmu.2021.628654
- https://doi.org//10.1080/15476286.2020.1857941
- https://doi.org//10.12659/msm.915555
- https://doi.org//10.1016/j.freeradbiomed.2015.12.027
- https://doi.org//10.1038/s41586-019-1471-1
- https://doi.org//10.1128/cmr.00035-19
- https://doi.org//10.1159/000487464
- https://doi.org//10.1002/jcb.27052
- https://doi.org//10.1097/PPO.0b013e318250c001
- https://doi.org//10.1002/jcp.27396
- https://doi.org//10.3390/genes11020172
- https://doi.org//10.1016/j.gene.2016.08.012
- https://doi.org//10.2478/jtim-2019-0002
- https://doi.org//10.3389/fimmu.2018.02847
- https://doi.org//10.1177/1759720x18776224
- https://doi.org//10.1080/15384101.2019.1671716
- https://doi.org//10.1002/art.38975
- https://doi.org//10.1016/j.ijpharm.2021.121137
- https://doi.org//10.1016/j.cell.2011.07.014
- https://doi.org//10.1089/jir.2018.0117
- https://doi.org//10.1155/2015/848790
- https://doi.org//10.1007/s10238-013-0271-4
- https://doi.org//10.1042/bsr20182374
- https://doi.org//10.1155/2020/6473858
- https://doi.org//10.1155/2020/5872980
- https://doi.org//10.1016/j.intimp.2018.09.049
- https://doi.org//10.1016/j.autrev.2015.05.004
- https://doi.org//10.3892/ijmm.2018.3632
- https://doi.org//10.1186/s12865-019-0297-9
- https://doi.org//10.2147/dddt.S90147
- https://doi.org//10.3892/ijmm.2019.4328
- https://doi.org//10.1172/jci97965
- https://doi.org//10.3389/fvets.2020.587273