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
Hepatobiliary Surgery Department, Guangxi Medical University Cancer Hospital, He Di Rd. #71, Nanning, 530021, People's Republic of China.
YanAn Hospital Affiliated to Kunming Medical University, Kunming, 650051, China.
Clin Transl Oncol. 2025 Apr;27(4):1612-1622. doi: 10.1007/s12094-024-03730-y. Epub 2024 Sep 19.
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.
研究长链非编码RNA lncSNHG16在肝细胞癌（HCC）中的表达，其表达与患者生存之间的关联，以及其在该疾病中调节自噬的潜在作用。
使用定量实时PCR检测培养的HCC细胞和患者的HCC组织中lncSNHG16的表达。在HCC培养物中，通过细胞增殖、伤口愈合、迁移或Transwell小室侵袭试验检测lncSNHG16过表达的影响。还在小鼠皮下肿瘤中检测lncSNHG16过表达的影响。使用蛋白质印迹法和流式细胞术探讨HCC培养物中lncSNHG16表达与自噬和凋亡的关系。
HCC组织中较高的lncSNHG16表达与患者总体生存率和无复发生存率显著较差相关。在HCC细胞培养物中过表达lncSNHG16可促进细胞增殖、迁移和侵袭，同时抑制凋亡。lncSNHG16与STAT3上调以及自噬和相关凋亡的抑制有关。在小鼠中过表达lncSNHG16可加速肿瘤生长和增加肿瘤重量。
非编码RNA lncSNHG16抑制HCC中的自噬和相关凋亡，使其成为潜在的治疗靶点。
