Inflammation-Induced Long Intergenic Noncoding RNA (LINC00665) Increases Malignancy Through Activating the Double-Stranded RNA-Activated Protein Kinase/Nuclear Factor Kappa B Pathway in Hepatocellular Carcinoma.
paper
Cited
Public
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- Authors
- Ding, Jie; Zhao, Jingjing; Huan, Lin; Liu, Yizhe; Qiao, Yejun; Wang, Zhen; Chen, Zhiao; Huang, Shenglin; Zhao, Yingjun; He, Xianghuo
- Year
- 2020
- Journal
- Hepatology (Baltimore, Md.)
- PMID
- 32083756
- DOI
- 10.1002/hep.31195
BACKGROUND AND AIMS: The nuclear factor kappa B (NF-ΞΊB) signaling pathway is important for linking inflammation and tumorigenesis. Here, we characterized an NF-ΞΊB signaling activation-induced long intergenic noncoding (LINC) RNA in hepatocellular carcinoma (HCC), LINC00665, that contributes to the enhanced cell proliferation of HCC cells both in vitro and in vivo. APPROACH AND RESULTS: LINC00665 physically interacts with the double-stranded RNA (dsRNA)-activated protein kinase (PKR), enhances its activation, and maintains its protein stability by blocking ubiquitin/proteasome-dependent degradation, resulting in a positive feedback regulation of NF-ΞΊB signaling in HCC cells. Notably, patients with HCC and higher LINC00665 have poorer outcomes in the clinic. CONCLUSIONS: Our findings indicate that LINC00665 is involved in the NF-ΞΊB signaling activation in HCC cells and that the inflammatory LINC00665/PKR/NF-ΞΊB loop plays important oncogenic roles in hepatic cancer progression and may be a potential therapeutic target.
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External
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