| Literature DB >> 29872866 |
Haiyun Qian1, Li Chen2, Jiangping Huang1, Xianghui Wang1, Shengwei Ma1, Fenghe Cui1, Liyun Luo3, Li Ling3, Kai Luo4, Guopei Zheng5.
Abstract
Recently, emerging evidence has suggested that long noncoding RNAs (lncRNAs) have crucial roles in cancer progression. Here, we demonstrated that the lncRNA MIR4435-2HG was highly expressed in lung cancer tissues and correlated with histological grades and lymph node metastasis. Phenotypic analysis indicated that MIR4435-2HG knockdown inhibited lung cancer cell proliferation and invasion in vitro and in vivo. Notably, MIR4435-2HG knockdown suppressed the EMT (epithelial-mesenchymal transition) process and cancer stem cell traits of lung cancer cells. Mechanistically, MIR4435-2HG knockdown decreased the transactivation of β-catenin. MIR4435-2HG interacted with β-catenin and thus prevented its degradation by the proteasome system. Our findings highlight the important roles and mechanisms of MIR4435-2HG in lung cancer progression. High expression of lncRNA MIR4435-2HG correlates with lung cancer progression MIR4435-2HG promotes lung cancer cells proliferation and invasion MIR4435-2HG knockdown suppresses the EMT process and cancer stem cell traits MIR4435-2HG knockdown inhibits the β-catenin signalling.Entities:
Keywords: EMT; Lung cancer; lncRNAs; β-catenin
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Year: 2018 PMID: 29872866 DOI: 10.1007/s00109-018-1654-5
Source DB: PubMed Journal: J Mol Med (Berl) ISSN: 0946-2716 Impact factor: 4.599