Evidence has shown the importance of long non-coding RNAs (IncRNAs) during angiogenesis and lung cancer progression. However, the potential functions of TNK2-AS1 in non-small cell lung cancer (NSCLC) remain elusive. By IncRNA profiling, we identified TNK2-AS1 as a novel oncogenic IncRNA in NSCLC. TNIQ-AS1 was significantly upregulated in NSCLC and correlated with poor prognosis. We found that TNK2-AS1 could increase viability and migration of NSCLC cells in vitro. TNK2-AS1 also promoted NSCLC xenograft tumor growth and metastasis in vivo. TNK2-AS1 could interact with STAT3 to increase its protein stability by protecting it from proteasome-mediated degradation. STAT3 could also bind TNK2-AS1 promoter to trigger its transcription. The positive feedback loop between STAT3 and TNK2-AS1 therefore augmented STAT3 signaling by elevating VEGFA expression to facilitate angiogenesis. Collectively, our work has elucidated a novel mechanism of TNIQ-AS1-mediated angiogenesis by enforcing STAT3/VEGFA signaling and may provide a potential target for therapeutic intervention. (C) 2018 Elsevier Inc. All rights reserved.
[1]Jilin Univ, China Japan Union Hosp, Dept Thorac Surg, Changchun 130033, Jilin, Peoples R China.
[2]Jilin Univ, China Japan Union Hosp, Dept Vasc Surg, Changchun 130033, Jilin, Peoples R China.
[3]Jilin Univ, Hosp 1, Changchun 130021, Jilin, Peoples R China.
[4]Jilin Univ, China Japan Union Hosp, Hlth Examinat Ctr, 126 Xiantai St, Changchun 130033, Jilin, Peoples R China.
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