A Positive Feedback Loop Involving the LINC00346/β-Catenin/MYC Axis Promotes Hepatocellular Carcinoma Progression

2019 ◽  
Author(s):  
Nuobei Zhang ◽  
Xin Chen
Hepatology ◽  
2019 ◽  
Vol 70 (4) ◽  
pp. 1214-1230 ◽  
Author(s):  
Shao‐Lai Zhou ◽  
Dan Yin ◽  
Zhi‐Qiang Hu ◽  
Chu‐Bin Luo ◽  
Zheng‐Jun Zhou ◽  
...  

2015 ◽  
Vol 5 (2) ◽  
pp. e1074376 ◽  
Author(s):  
Ang Lin ◽  
Guan Wang ◽  
Huajun Zhao ◽  
Yuyi Zhang ◽  
Qiuju Han ◽  
...  

2019 ◽  
Vol 515 (3) ◽  
pp. 455-461 ◽  
Author(s):  
Ming Han ◽  
Hongping Lu ◽  
Kai Han ◽  
Xiaoxue Yuan ◽  
Shunai Liu ◽  
...  

2017 ◽  
Vol 60 (6) ◽  
pp. 617-626 ◽  
Author(s):  
Shuran Li ◽  
Xueyang Bao ◽  
Duowei Wang ◽  
Linjun You ◽  
Xianjing Li ◽  
...  

Author(s):  
Bin Zhu ◽  
Jun-Jie Chen ◽  
Ying Feng ◽  
Jun-Ling Yang ◽  
Hua Huang ◽  
...  

Abstract Background Angiogenesis plays an important role in the occurrence, development and metastasis of hepatocellular carcinoma (HCC). According to previous studies, miR-378a participates in tumorigenesis and tumor metastasis, but its exact role in HCC angiogenesis remains poorly understood. Methods qRT-PCR was used to investigate the expression of miR-378a-3p in HCC tissues and cell lines. The effects of miR-378a-3p on HCC in vitro and in vivo were examined by Cell Counting Kit-8 (CCK-8), Transwell, tube formation and Matrigel plug assays, RNA sequencing, bioinformatics, luciferase reporter, immunofluorescence and chromatin immunoprecipitation (ChIP) assays were used to detect the molecular mechanism by which miR-378a-3p inhibits angiogenesis. Results We confirmed that miR-378a-3p expression was significantly downregulated and associated with higher microvascular density (MVD) in HCC; miR-378a-3p downregulation indicated a short survival time in HCC patients. miR-378a-3p knockdown led to a significant increase in angiogenesis in vitro and in vivo. We found that miR-378a-3p directly targeted TNF receptor associated factor 1 (TRAF1) to attenuate NF-κB signaling, and then downregulated secreted vascular endothelial growth factor. DNA methyltransferase 1 (DNMT1)-mediated hypermethylation of miR-378a-3p was responsible for downregulating miR-378a-3p. Moreover, a series of investigations indicated that p65 initiated a positive feedback loop that could upregulate DNMT1 to promote hypermethylation of the miR-378a-3p promoter. Conclusion Our study indicates a novel DNMT1/miR-378a-3p/TRAF1/NF-κB positive feedback loop in HCC cells, which may become a potential therapeutic target for HCC.


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