lncSNHG16 promotes hepatocellular carcinoma development by inhibiting autophagy
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Zhu Jian Deng [1] ; Hao Tian Liu [1] ; Bao Hong Yuan [2] ; Li Xin Pan [1] ; Yu Xian Teng [1] ; Jia Yong Su [1] ; Cheng Piao Luo [1] ; Ping Ping Guo [1] ; Jian Hong Zhong [1]
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[1] Guangxi Medical University
Guangxi Medical University
China
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[2] Kunming Medical University
Kunming Medical University
China
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- Localización: Clinical & translational oncology, ISSN 1699-048X, Vol. 27, Nº. 4, 2025, págs. 1612-1622
- Idioma: inglés
- Texto completo no disponible (Saber más ...)
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Resumen
Objective 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.
Methods Expression of lncSNHG16 was measured using quantitative real-time PCR in HCC cells in culture and HCC tissues from patients. Efects of lncSNHG16 overexpression were examined in HCC cultures using assays of cell proliferation, wound healing, and migration or invasion in Transwell dishes. Efects 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 fow cytometry.
Results Higher lncSNHG16 expression in HCC tissues was associated with signifcantly 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.
Conclusion The non-coding RNA lncSNHG16 suppresses autophagy and associated apoptosis in HCC, making it a potential therapeutic target.
