CircRNA_0084043 acts as a competitive endogenous RNA promotes osteosarcoma progression by sponging miR-153

Zhang, Baode; Teng, Xuli; Yang, Weidong; Yang, Enqin; Li, Hongmei; Jing, Shenfeng

doi:10.23736/s0026-4806.20.07229-8

Cited by 2 publications

(1 citation statement)

References 5 publications

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“…Our analysis revealed that circADAM9 (circBase ID: hsa_circ_0084043) has several potential binding sites for miR-545-3p. CircADAM9 plays an oncogenic role by regulating the proliferation, apoptosis, migration, and invasion of cancer cells in melanoma [14][15][16] and osteosarcoma [17]. CircADAM9 has also been implicated in diabetic retinopathy and is involved in the regulation of retinal pigment epithelial cell damage, including cell proliferation, apoptosis, inflammation, and oxidative stress [18][19][20].…”

Section: Introductionmentioning

confidence: 99%

Circular RNA circADAM9 Promotes Inflammation, Oxidative Stress, and Fibrosis of Human Mesangial Cells via the Keap1-Nrf2 Pathway in Diabetic Nephropathy

Zheng

Liu

Song

2023

Exp Clin Endocrinol Diabetes

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Objective Circular RNAs (circRNAs) have been discovered as potential biomarkers for diabetic nephropathy (DN). In this study, the potential roles of circADAM9 in high glucose (HG)-induced cell injury of human mesangial cells (HMCs) were investigated, and the underlying mechanism was elucidated. Methods DN cell model in vitro was simulated by HG treatment of HMCs. Endogenous expressions of circADAM9, miR-545-3p, and ubiquitin-specific protease 15 (USP15) were determined by real-time polymerase chain reaction. Cell proliferation and migration were evaluated using Cell Counting Kit-8 and wound healing assays. The inflammatory response was assessed by enzyme-linked immunosorbent assay. Oxidative stress was examined using commercially available kits. Dual-luciferase reporter and RNA pull-down assays were conducted to confirm the interaction among circADAM9, miR-545-3p, and USP15. Results CircADAM9 was upregulated in DN samples and HG-treated HMCs, while its downregulation inhibited cell proliferation, inflammation, fibrosis, and oxidative stress. Further investigation revealed that circADAM9 exerted this influence by targeting the miR-545-3p/USP15 axis, thereby regulating the KELCH-like ECh-associated protein 1/nuclear factor erythroid 2 related factor 2 (Keap1/Nrf2) pathway. MiR-545-3p knockdown or USP15 overexpression reversed the effect of circADAM9 silencing in HG-induced HMCs. Conclusion These results indicate that the circADAM9/miR-545-3p/USP15/Keap1/Nrf2 signaling axis is critical for HG-induced cell injury in HMCs and might represent a novel therapeutic target for DN treatment.

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