A1BG-AS1 promotes the biological functions of osteosarcoma cells via regulating the microRNA-148a-3p/USP22 axis and stabilizing the expression of SIRT1 through deubiquitinase function

ABSTRACTBackground The study aims to explore the role of A1BG antisense RNA 1 (A1BG-AS1), microRNA (miR)-148a-3p and ubiquitin-specific protease 22 (USP22) on osteosarcoma (OS) cell growth.Research design & methods A1BG-AS1, miR-148a-3p, USP22, and silent information regulator 2 homolog 1 (SIRT1) levels in OS tissues and cells were determined. The effects of A1BG-AS1, miR-148a-3p, and USP22 on the biological functions of OS cells were examined by functional assays. In vivo assay was conducted to observe the effect of A1BG-AS1 on OS growth in vitro. The relationship of A1BG-AS1, miR-148a-3p, and USP22 was analyzed by bioinformatics analysis, RNA-fluorescence in situ hybridization, luciferase activity, and RNA binding protein immunoprecipitation assays. The relation between USP22 and SIRT1 was evaluated by immunoprecipitation.Results A1BG-AS1 and USP22 were highly expressed, and miR-148a-3p was lowly expressed in OS tissues and cells. Down-regulation of A1BG-AS1 and USP22 or up-regulation of miR-148a-3p impaired the malignant behaviors of OS cells. A1BG-AS1 sponged miR-148a-3p, and miR-148a-3p targeted USP22, thereby inhibiting USP22 expression. Up-regulating USP22 reversed the A1BG-AS1 suppression-induced phenotypic inhibition of OS cells. USP22 affected the biological functions of OS cells by deubiquitinating SIRT1.Conclusion A1BG-AS1 facilitates the biological functions of OS cells via mediating the miR-148a-3p/USP22 axis.KEYWORDS: Osteosarcomalong non-coding RNA A1BG antisense RNA 1microRNA-148a-3pubiquitin-specific protease 22silent information regulator 2 homolog 1deubiquitination Declaration of interestsThe authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.Reviewer disclosuresPeer reviewers on this manuscript have no relevant financial or other relationships to disclose.Author contributionsXiuxin Han and Lili Li contributed to study design; Mengfan Yin and Guowen Wang contributed to manuscript editing; Chen Gong, Chao Zhang, and Genbao Zhu contributed to experimental studies; Mengxue Hu, Kemeng Tan, and La Jiang contributed to data analysis. All authors read and approved the final manuscript.Data availability statementThe data that support the findings of this study are available from the corresponding author upon reasonable request.Supplementary materialSupplemental data for this article can be accessed online at https://doi.org/10.1080/14728222.2023.2263908Additional informationFundingThis research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.