LINC00305 represses miR-124 expression to trigger inflammatory insults in the presence of lipopolysaccharide.

ABSTRACT

Background: The anti-inflammatory function of microRNA-124 (miR-124) has been a matter of extensive studies in the last few years. Although LINC00305 regulates biological activities by acting as a miR sponge, it is still unexplored whether LINC00305 is involved in inflammation by regulating miR-124. Methods: Cell viability and apoptosis were evaluated with commercial kits, cell counting kit-8 (CCK-8) and Annexin V-fluorescein isothiocyanate (FITC) kit, respectively. LINC00305, miR-124 and mRNA levels were quantified by quantitative reverse transcription PCR (qRT-PCR). Protein level was assessed with Western blot assay and enzyme-linked immunosorbent assay (ELISA). Results: The expression of LINC00305 was up-regulated by lipopolysaccharide (LPS). LINC00305 overexpression further suppressed the cell viability, promoted apoptosis and induced inflammation in LPS-treated ATDC5 cells while its silence enhanced the cell viability, inhibited apoptosis and ameliorated inflammation. miR-124 was negatively regulated by LINC00305 and its overexpression abolished the effects of LINC00305 in the presence of LPS. LINC00305 further triggered the Notch/nuclear factor kappa B (NF-κB) signalling pathway in LPS-treated ATDC5 cells and this activation was abrogated when ATDC5 cells overexpressed miR-124. Conclusion: LINC00305 might emerge as a novel suppressor for miR-124. LINC00305-caused miR-124 silence compromises ATDC5 cell viability and ultimately results in inflammatory insults by activating Notch/NF-κB pathway.