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- W4289745650 abstract "It is observed that circular RNA (circRNA) PTTG1 interacting protein (circPTTG1IP) level is notably up-regulated in rheumatoid arthritis (RA) patients by previous study. However, its precise role and working mechanism in RA pathology remain to be clarified.Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and Western blot assay were carried out to examine RNA and protein expression. Cell proliferation was analyzed by colony formation assay and 5-Ethynyl-2'-deoxyuridine (EdU) assay. Cell motility was assessed by transwell assays and wound healing assay. Flow cytometry (FCM) analysis was performed to assess cell apoptosis rate. Dual-luciferase reporter, RNA immunoprecipitation (RIP), and RNA-pull down assays were conducted to confirm the interaction between microRNA-431-5p (miR-431-5p) and circPTTG1IP or follistatin like 1 (FSTL1). CircPTTG1IP expression was up-regulated in the synovial tissues of RA patients and RA patients-derived fibroblast-like synoviocytes (RA-FLS). CircPTTG1IP absence suppressed the proliferation, migration, and invasion and induced the apoptosis of RA-FLS. CircPTTG1IP negatively regulated the expression of miR-431-5p by directly binding to it in RA-FLS. CircPTTG1IP interference-mediated effects in RA-FLS were largely counteracted by the silence of miR-431-5p. miR-431-5p directly interacted with the 3' untranslated region (3'UTR) of FSTL1. FSTL1 overexpression largely overturned miR-431-5p accumulation-mediated effects in RA-FLS. CircPTTG1IP positively regulated FSTL1 expression by sponging miR-431-5p in RA-FLS.CircPTTG1IP absence suppressed RA progression through mediating miR-431-5p/FSTL1 signaling cascade." @default.
- W4289745650 created "2022-08-04" @default.
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- W4289745650 date "2022-12-01" @default.
- W4289745650 modified "2023-09-30" @default.
- W4289745650 title "CircPTTG1IP knockdown suppresses rheumatoid arthritis progression by targeting miR-431-5p/FSTL1 axis" @default.
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- W4289745650 doi "https://doi.org/10.1016/j.trim.2022.101685" @default.
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