Silencing of long noncoding RNA SBF2-AS1 inhibits proliferation, migration and invasion and contributes to apoptosis in osteosarcoma cells by upregulating microRNA-30a to suppress FOXA1 expression.

Objectives: Long noncoding RNA (lncRNA) SBF2-AS1 was found to be related to some tumors. Nevertheless, the role of SBF2-AS1 in osteosarcoma (OS) is still needed to be elaborated. This study is conducted to examine the expression of lncRNA SBF2-AS1 in OS with the involvement of microRNA-30a (miR-30a) and FOXA1. Methods: OS tissues and its corresponding adjacent normal tissues were obtained for the detection of SBF2-AS1 expression and its relations with clinical phenotypes. OS cells with most significant expression of SBF2-AS1 were selected for subsequent experiments. Moreover, a series of experiments were performed to detect proliferation, invasion, migration, colony formation, cell cycle distribution and apoptosis of OS cells. Furthermore, the binding site between SBF2-AS1 and miR-30a as well as between miR-30a and FOXA1 was verified. Results: SBF2-AS1 was overexpressed in tissues and cells of OS. Additionally, silencing of SBF2-AS1 and miR-30a overexpression inhibited the proliferation, migration and invasion of OS cells and promoted their apoptosis. Moreover, lncRNA SBF2-AS1 regulated miR-30a by serving as a ceRNA, thus promoting FOXA1 expression. Furthermore, interfered SBF2-AS1 or upregulated miR-30a restrained the growth of OS. Conclusion: Our study confirms that silencing of SBF2-AS1 represses proliferation, migration and invasion of OS cells and promotes their apoptosis by binding to miR-30a and inhibiting FOXA1 expression.

Long noncoding RNA MALAT-1 inhibits apoptosis and matrix metabolism disorder in interleukin-1ß-induced inflammation in articular chondrocytes via the JNK signaling pathway.

Proinflammatory cytokine such as interleukin (IL)-1ß causes inflammation of articular cartilage. In this current study, we explored the chondroprotective effects of long noncoding RNA (lncRNA) MALAT-1 on cell proliferation, apoptosis, and matrix metabolism in IL-1ß-induced inflammation in articular chondrocytes. Articular chondrocytes from knee joints of normal rats were isolated and cultured, followed by identification through observation of toluidine blue and COL II immunocytochemical stainings. The proliferation of chondrocytes at passage 2 was detected by the 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay. The inflammatory chondrocytes induced by 10 ng/mL IL-1ß were observed and identified by toluidine blue and COL II immunocytochemical stainings. pcDNA 3.1 and pcDNA-MALAT-1 were transfected in the chondrocytes. Ultrastructure of chondrocytes was observed by using a transmission electron microscope. The MTT assay was carried out to evaluate chondrocyte viability. Hoechst 33258 staining and flow cytometry were adopted to assess chondrocyte apoptosis. The chondrocytes at passage 2 with the biological characteristics of chondrocytes were used for subsequent experiments. In IL-1ß-treated chondrocytes, the growth rate of chondrocytes slowed down, the cells became narrow and long, the vacuoles were seen in the cells, and the morphology of the chondrocytes was irregular. The toluidine blue staining and the immunohistochemical staining of COL II became weaker. In response to IL-1ß induction, articular chondrocytes showed reduced MALAT-1 expression; moreover, obvious cartilage injury was observed with decreased chondrocyte viability and Col II expression and elevated chondrocyte apoptosis, MMP-13 expression, and p-JNK expression. With the treatment of pcDNA-MALAT-1, the cartilage injury was alleviated with increased chondrocyte viability and type II collagen (Col II) expression and reduced chondrocyte apoptosis, MMP-13 expression and p-JNK expression. Taken together these results, lncRNA MALAT-1 blocked the activation of the JNK signaling pathway; thereby, IL-1ß-induced inflammation in articular chondrocytes was reduced with enhanced chondrocyte proliferation and suppressed chondrocyte apoptosis and extracellular matrix degradation.