lncSNHG16通过抑制自噬促进肝细胞癌的发展

Zhu-Jian Deng, Hao-Tian Liu, Bao-Hong Yuan, Li-Xin Pan, Yu-Xian Teng, Jia-Yong Su, Cheng-Piao Luo, Ping-Ping Guo, Jian-Hong Zhong
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摘要

目的研究长非编码RNA lncSNHG16在肝细胞癌(HCC)中的表达、其表达与患者存活率之间的关系,以及其在该疾病中调节自噬的潜在作用。方法采用定量实时PCR技术测定lncSNHG16在培养的HCC细胞和患者HCC组织中的表达。在HCC培养物中使用细胞增殖、伤口愈合和Transwell培养皿中的迁移或侵袭检测lncSNHG16过表达的影响。在小鼠皮下肿瘤中也检测了lncSNHG16过表达的影响。结果HCC组织中较高的lncSNHG16表达与患者较差的总生存期和无复发生存期有关。在HCC细胞培养中过表达lncSNHG16可促进细胞增殖、迁移和侵袭,同时抑制细胞凋亡。结论 非编码 RNA lncSNHG16 可抑制 HCC 中的自噬和相关凋亡,使其成为一个潜在的治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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lncSNHG16 promotes hepatocellular carcinoma development by inhibiting autophagy

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. 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.

Results

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.

Conclusion

The non-coding RNA lncSNHG16 suppresses autophagy and associated apoptosis in HCC, making it a potential therapeutic target.

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