lncSNHG16 promotes hepatocellular carcinoma development by inhibiting autophagy

• Published in: Clinical & translational oncology
• Main Authors: Deng, Zhu-Jian, Liu, Hao-Tian, Yuan, Bao-Hong, Pan, Li-Xin, Teng, Yu-Xian, Su, Jia-Yong, Luo, Cheng-Piao, Guo, Ping-Ping, Zhong, Jian-Hong
• Format: Journal Article
• Language: English
• Published: Italy 19.09.2024
• Subjects: lncSNHG16; Hepatocellular carcinoma; Autophagy
• ISSN: 1699-3055; 1699-3055
• DOI: 10.1007/s12094-024-03730-y

To investigate the expression of long non-coding RNA lncSNHG16 in hepatocellular carcinoma (HCC), associations between its expression and patient survival, and its potential role in regulating autophagy in the disease. Expression of lncSNHG16 was measured using quantitative real-time PCR in HCC cells in culture and HCC tissues from patients. Effects of lncSNHG16 overexpression were examined in HCC cultures using assays of cell proliferation, wound healing, and migration or invasion in Transwell dishes. Effects of lncSNHG16 overexpression were also examined in subcutaneous tumor in mice. Relationships of lncSNHG16 expression to autophagy and apoptosis in HCC cultures were explored using western blotting and flow cytometry. Higher lncSNHG16 expression in HCC tissues was associated with significantly worse overall and recurrence-free survival of patients. Overexpressing lncSNHG16 in HCC cell culture promoted cell proliferation, migration, and invasion while suppressing apoptosis. lncSNHG16 was associated with upregulation of STAT3 as well as inhibition of autophagy and associated apoptosis. Overexpressing lncSNHG16 accelerated tumor growth and weight in mice. The non-coding RNA lncSNHG16 suppresses autophagy and associated apoptosis in HCC, making it a potential therapeutic target.