MYC-activated lncRNAHNF1A-AS1overexpression facilitates glioma progression via cooperating withmiR-32-5p/SOX4axis

Mounting literatures have revealed the crucial effects of long noncoding RNA (lncRNA) in various cancers, including glioma.HNF1A-AS1, a novel lncRNA, is reported to modulate tumorigenesis and development of multiple cancers. However, the tumorigenic function of lncRNAHNF1A-AS1in glioma remains largely unknown. quantitative reverse transcription and polymerase chain reaction and western blot assays were applied to evaluate the expression of relevant mRNAs and proteins. 5-Ethynyl-2'- deoxyuridine, terminal deoxynucleotidyl transferase dUTP nick-end labeling, flow cytometry, and transwell assays were conducted for examining the influence ofHNF1A-AS1on glioma cell functions. The relationship among RNAs was investigated by mechanical experiments. The results demonstrated thatHNF1A-AS1was predominantly highly expressed in glioma cell lines compared with nontumor glial epithelial cell, which was associated with the stimulation of transcription factor myelocytomatosis oncogene. Knockdown ofHNF1A-AS1remarkably inhibited glioma cells proliferation, migration, and invasion, while accelerating cell apoptosis in vitro. Mechanically,HNF1A-AS1served as amiR-32-5psponge. Moreover,SOX4was discovered as a target ofmiR-32-5p. InhibitedmiR-32-5por upregulatedSOX4could markedly counteract the inhibitory effects of silencingHNF1A-AS1on glioma malignant biological behaviors.HNF1A-AS1exerted oncogenic property in glioma progression via upregulatingmiR-32-5p-mediatedSOX4expression, suggesting potential novel therapeutic target for future glioma treatment.