Abstract
Long non-coding RNA small nucleolar RNA host gene 7 (SNHG7) is involved in a variety of different types of cancer; however, the role of SNHG7 during liver cancer progression is not completely understood. The aim of the present study was to investigate the functional role and regulatory mechanism underlying SNHG7 during liver cancer. A total of 25 paired hepatocellular carcinoma (HCC) tumor tissues and adjacent normal tissues were collected. Reverse transcription-quantitative PCR and western blotting were performed to detect the expression levels of SNHG7, microRNA (miR)-34a, sirtuin 1 (SIRT1) and pyroptosis-related targets. RNA fluorescence in situ hybridization was performed to detect the expression of SNHG7 in HCC tissues. SNHG7 expression was upregulated in HCC tissues and liver cancer cells compared with normal tissues and normal liver cell lines. High expression of SNHG7 inhibited NLR family pyrin domain containing 3 (NLRP3)-dependent pyroptosis in HepG2 and SK-hep-1 cells. Bioinformatics analysis and dual-luciferase reporter assays were performed to investigate the interactions between miR-34a and SNHG7 or SIRT1. SNHG7 served as a competing endogenous RNA of miR-34a, and SIRT1 was identified as a direct target of miR-34a. Cell pyroptosis was evaluated by TUNEL and lactate dehydrogenase release assays. SNHG7 knockdown reduced SIRT1 expression, but increased the expression levels of NLRP3, caspase-1 and interleukin-1β, leading to pyroptosis. SNHG7 knockdown-induced effects were enhanced by miR-34a upregulation. In summary, the present study indicated that the SNHG7/miR-34a/SIRT1 axis contributed to NLRP3-dependent pyroptosis during liver cancer.