Circular RNA hsa_circ_0005567 overexpression promotes M2 type macrophage polarization through miR-492/SOCS2 axis to inhibit osteoarthritis progression

Circular RNAs (circRNAs) can regulate the progression of osteoarthritis (OA) via serving as competing endogenous RNAs (ceRNAs). This work was performed for functional research of circ_0005526 in Interleukin-1β (IL-1β)-induced OA injury. Circ_0005526, microRNA-142-5p (miR-142-5p) or transcription factor 4 (TCF4) expression was measured via reverse transcription-quantitative polymerase chain reaction assay. Cell analysis was performed by Cell Counting Kit-8 assay for cell viability, EdU assay for cell proliferation and flow cytometry for cell apoptosis. The protein level detection was conducted using western blot. Target analysis was carried out via dual-luciferase reporter assay and RNA pull-down assay. Circ_0005526 was upregulated in OA cartilage tissues and IL-1β-exposed chondrocyte cells. IL-1β inhibited cell viability and proliferation but enhanced cell apoptosis and inflammation, then these damages were attenuated after downregulation of circ_0005526. Circ_0005526 interacted with miR-142-5p, and circ_0005526 knockdown suppressed IL-1β-induced OA progression through upregulating miR-142-5p. TCF4 was regulated by circ_0005526 via targeting miR-142-5p. The function of circ_0005526 was also achieved by upregulation of TCF4. These results unraveled that circ_0005526 promoted IL-1β-induced chondrocyte injury in OA via suppressing miR-142-5p binding to TCF4.

Section: Discussionmentioning

confidence: 99%

Circ_0005526 contributes to interleukin-1β-induced chondrocyte injury in osteoarthritis via upregulating transcription factor 4 by interacting with miR-142-5p

Wahafu

Tuo

et al. 2022

“…Then, miR-107 mimics or NC mimics was co-transfected with the above reporters into HFWT and 17–94 cells. After 48 h co-transfection, the Dual-Luciferase Reporter Assay System (Promega, USA) was utilized to evaluate luciferase activities [ 23 ].…”

Section: Methodsmentioning

confidence: 99%

CircSLC7A6 promotes the progression of Wilms’ tumor via microRNA-107/ ABL proto-oncogene 2 axis

Hao

Gao

et al. 2022

The dysregulation of circular RNAs (circRNAs) has been proved to be involved in the carcinogenesis of various cancers. Nevertheless, the biological function of circSLC7A6 remains unclear in Wilms’ tumor (WT). In our study, we found that circSLC7A6 was upregulated in cancerous WT tissues and cells. Cell apoptosis was increased while cell viability, migration, and invasion were repressed by circSLC7A6 silencing. Besides, circSLC7A6 knockdown suppressed WT tumor growth in vivo . miR-107 was identified as a direct target of circSLC7A6, and circSLC7A6 could negatively regulate miR-107 expression. In addition, circSLC7A6 knockdown inhibited WT progression, while the effect was partially abolished by the downregulation of miR-107. Additionally, ABL proto-oncogene 2 axis (ABL2) was verified as a downstream gene of miR-107, and circSLC7A6 could upregulate ABL2 expression by serving as a ceRNA of miR-107. Moreover, functional assays revealed that ABL2 overexpression reversed the impact of circSLC7A6 depletion on cell proliferation, migration, invasion, and apoptosis of WT. In conclusion, the present study demonstrated that circSLC7A6 facilitated WT progression by upregulating ABL2 through inhibiting miR-107 expression. These results suggested that circSLC7A6 might serve as a potential therapeutic target for WT.

“…The luciferase reporter plasmids containing ARAP1 promoter were transfected with EZH2-shRNA and EZH2-vector into A549 and H1975 cells using Lipofectamine 2000 (Invitrogen). The ratio of firefly to renilla luciferase activity was detected as the luciferase activity using the dual-luciferase reporter assay system (Promega, Madison, WI, USA) 48 h later [ 31 ].…”

Section: Methodsmentioning

confidence: 99%

Long noncoding RNA ArfGAP with RhoGAP domain, ankyrin repeat and PH domain 1 antisense RNA 1 recruits enhancer of zeste 2 polycomb repressive complex 2 subunit to promote the proliferation, migration and invasion of lung adenocarcinoma cells

Liu¹,

Pan²,

Lu³

et al. 2022

The detailed function of ARAP1-AS1, the antisense RNA of Arf-GAP with Rho-GAP domain, ANK repeat and PH domain-containing protein 1 (ARAP1), in lung adenocarcinoma (LUAD) has not been clearly elucidated and required further investigation. Our study is committed to exploring the role of ARAP1-AS1 in LUAD. Gene expression in LUAD was measured by real-time quantitative polymerase-chain reaction (RT-qPCR). The influence of ARAP1-AS1 on LUAD cell malignant behaviors was evaluated by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, colony formation assay, Transwell invasion assay and wound healing assay. Subcellular fractionation assay detected the cellular localization of ARAP1-AS1 in LUAD. The protein levels were subjected to western blotting. RNA immunoprecipitation (RIP) and luciferase reporter assay were employed to verify the interaction between ARAP1-AS1, ARAP1 and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2). Our investigation identified that ARAP1-AS1 was upregulated in LUAD cells and tissues. ARAP1-AS1 silencing repressed LUAD cell growth and migration. Furthermore, ARAP1-AS1 knockdown altered the expression of its sense mRNA, ARAP1. ARAP1-AS1 could recruit EZH2 to inhibit ARAP1 expression. Additionally, the downregulation of ARAP1 reversed ARAP1-AS1 downregulation-induced repression of cell growth and migration in LUAD. In conclusion, ARAP1-AS1 recruited EZH2 to silence ARAP1, facilitating cell proliferation, migration and invasion in LUAD. Our study demonstrated the possibility of ARAP1-AS1 to be a novel therapeutic target for LUAD.