LncRNA-GAS5 Inhibits Expression of miR 103 and Ameliorates the Articular Cartilage in Adjuvant-Induced Arthritis in Obese Mice.

We explored whether long noncoding RNA growth arrest-specific transcript 5 (LncRNA-GAS5) small interfering RNA (siRNA) reduced cartilage destruction in obese mice with adjuvant-induced arthritis. We studied the effects of LncRNA-GAS5 siRNA on the polyarthritis index; hind paw swelling; and the serum levels of certain biochemicals, cytokines, and oxidative stress parameters. We measured the expression levels of matrix metalloproteinases (MMP)-13, NF-κB, fibroblast growth factor (FGF) 21, p38, Akt, and PI3K in cartilage via Western blotting and quantitative reverse transcription PCR. Long noncoding RNA-GAS5 siRNA reduced joint swelling; the serum levels of arthritis-associated biochemicals, cytokines, and oxidative stress markers; and cartilage MMP-13, NF-κB, FGF21, p38, Akt, and PI3K levels. Cartilage miR-103 expression was reduced. Histopathologically, LncRNA-GAS5 siRNA ameliorated the pathological changes of cartilage. Long noncoding RNA-GAS5 siRNA prevented cartilage destruction by inhibiting miR-103 expression.

miR-106b-5p promotes cell proliferation and cell cycle progression by directly targeting CDKN1A in osteosarcoma.

MicroRNA (miR)-106b-5p has been reported to act as both an oncogene and tumor suppressor in several tumors. The aim of the present study was to investigate the biological function of miR-106b-5p in osteosarcoma (OS). miR-106b-5p expression was observed to be significantly increased in OS tissues and cell lines. MTT assay and flow cytometry analysis determined that miR-106b-5p inhibitor transfection suppressed OS cell proliferation and induced cell cycle G0/G1 phase arrest. Furthermore, bioinformatics analysis and a luciferase reporter assay demonstrated that cyclin-dependent kinase inhibitor 1A (CDKN1A) was a potential target of miR-106b-5p. p21 protein expression was found to be significantly increased by miR-106b-5p downregulation in OS cells. Further analysis demonstrated that CDKN1A was downregulated in OS tissues and was negatively correlated with miR-106b-5p expression. Furthermore, upregulation of CDKN1A expression mimicked, whilst CDKN1A knockdown reversed the suppressive effects of miR-106b-5p inhibitor on OS cell proliferation and cell cycle progression. In summary, the present data suggested that miR-106b-5p promotes cell proliferation and cell cycle progression by directly targeting CDKN1A in OS.