Objective: Our study aimed to probe the potential molecular mechanism of long non ⁃ coding RNA (lncRNA) VIM Antisense RNA 1 (VIM⁃AS1) in diabetic retinopathy. Methods: LncRNA VIM⁃AS1, miR⁃497⁃5p and FBXW7 mRNA expressions were determined using qRT⁃PCR. The FBXW7 protein level was also detected using western blotting. The cell viability, migration and apoptosis were evaluated using CCK⁃8 assay, wound healing assay and flow cytometry analysis, respectively. Additionally, the binding relationships among lncRNA VIM⁃AS1, miR⁃497⁃5p and FBXW7 were verified by dual luciferase reporter assaies. Results: LncRNA VIM⁃AS1 and FBXW7 expressions were remarkably reduced in HG⁃treated ARPE⁃19 cells, while miR⁃497⁃5p was upregulated. LncRNA VIM ⁃ AS1 could upregulate the expression of FBXW7 by competitively binding to miR ⁃ 497 ⁃ 5p. LncRNA VIM ⁃ AS1 overexpression promoted cell proliferation and migration, and inhibited cell apoptosis in HG⁃induced ARPE⁃19 cells, while miR⁃497⁃ 5p overexpression abolished the effects of lncRNA VIM⁃AS1 overexpression on HG⁃induced ARPE⁃19 cells. Furthermore, FBXW7 knockdown abrogated the effects of miR⁃497⁃5p inhibition on cell phenotypes of HG⁃treated ARPE⁃19 cells. Conclusion: LncRNA VIM⁃AS1 could promote the proliferation and migration, while inhibited cell apoptosis of HG⁃treated ARPE⁃19 cells by regulation of miR⁃497⁃5p/FBXW7 axis, suggesting that lncRNA VIM⁃AS1 might have great potential as therapeutic target for diabetic retinopathy. [ABSTRACT FROM AUTHOR]