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Long non-coding RNA actin filament-associated protein 1- antisense RNA 1 mediates breast cancer cell proliferation and migration through the miR-21/PTEN axis
- Publication Year :
- 2022
- Publisher :
- Research Square Platform LLC, 2022.
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Abstract
- Background LncRNAs take various effects mostly through sponging with miRNAs. Based on public databases and integrating bioinformatics analyses and further validated in BC tissue and cell lines, the effect of lncRNA AFAP1-AS1 on breast cancer cells proliferation and migration was verified and might work via miR-21/PTEN axis. Methods The expression of AFAP1-AS1, miR-21, PTEN in BC tissues and cell lines were analyzed by qRT-PCR. BC cell proliferation and migration were examined using EdU, colony formation assays and wound healing, transwell assays, respectively. The cellular localization of AFAP1-AS1 was analyzed using FISH. RNA pull down assay was performed to analyze the binding of AFAP1-AS1 to miR-21. The interaction between miR-21 and PTEN was examined using a dual luciferase reporter assay. The effect of AFAP1-AS1 on BC tumor growth in vivo was analyzed using a tumor xenograft mouse model. Results The expression of AFAP1-AS1, which was significantly upregulated in BC tissues and cell lines. The higher expression of AFAP1-AS1 was correlated with old age and lymph node metastasis of patients with BC. AFAP1-AS1 knockdown BC cells exhibited decreased proliferation and migration in vitro and in vivo. Additionally, AFAP1-AS1 knockdown downregulated miR-21 expression and upregulated PTEN expression. Mechanistically, the interaction between AFAP1-AS1 and miR-21 promotes BC cell proliferation and migration. AFAP1-AS1 knockdown decreased BC cell proliferation and migration, which are regulated by PTEN, through miR-21 regulation. Conclusions The knockdown of lncRNA AFAP1-AS1 upregulated PTEN expression and consequently attenuated miR-21-mediated enhanced BC cell proliferation and migration. LncRNA AFAP1-AS1 is a potential prognostic biomarker for BC patients.
Details
- Database :
- OpenAIRE
- Accession number :
- edsair.doi...........d42ecd54948a58d2a11adf8d4f1fca87