• Haiyun Qian, Li Chen, Jiangping Huang, Xianghui Wang, Shengwei Ma, Fenghe Cui, Liyun Luo, Li Ling, Kai Luo, and Guopei Zheng.
• Department of Cardiothoracic Surgery, Jingzhou Central Hospital, The Second Clinical Medical College, Yangtze University, Renming Road 1#, Jingzhou, 434020, Hubei, China.
• J. Mol. Med. 2018 Aug 1; 96 (8): 753-764.

AbstractRecently, 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.

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