MYC ‐activated lncRNA HNF1A‐AS1 overexpression facilitates glioma progression via cooperating with miR‐32‐5p/SOX4 axis

SilencingHNF1A ‐AS1 dampens glioma cell proliferation, migration, and invasion, while facilitating apoptosis. Myelocytomatosis oncogene induces overexpression ofHNF1A ‐AS1 via transcription activation.HNF1A ‐AS1 directly binds tomiR ‐32‐5p andmiR ‐32‐5p inhibition could reverse the restraining effects ofHNF1A ‐AS1 knockdown on glioma. AbstractMounting 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 ‐AS1 in 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 ‐AS1 on glioma cell functions. The relationship among RNAs was investigated by mechanical experiments. The results demonstrated thatHNF1A ‐AS1 was 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 ‐AS1 remarkably inhibited glioma cells proliferation, migration, and invasion, while accelerating cell apopt...
Source: Cancer Medicine - Category: Cancer & Oncology Authors: Tags: ORIGINAL RESEARCH Source Type: research