Silencing of lncRNA AFAP1-AS1 suppressed lung cancer development by regulatory mechanism in cis and trans
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Baoying Peng1,2,*, Anfei Liu2,*, Xuanwei Yu2,*, Enwu Xu3, Jiabin Dai2, Mengcheng Li2 and Qiaoyuan Yang1,2
1The State Key Lab of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Yuexiu District, Guangzhou 510120, PR China
2The Institute for Chemical Carcinogenesis, Guangzhou Medical University, Xinzao, Panyu District, Guangzhou 511436, PR China
3Department of Thoracic Surgery, General Hospital of Guangzhou Military Command of Chinese People’s Liberation Army, Guangzhou 510010, PR China
*These authors have contributed equally to this work
Qiaoyuan Yang, email: email@example.com
Keywords: long noncoding RNA, AFAP1-AS1, lung cancer, natural antisense transcripts, AFAP1
Received: May 30, 2017 Accepted: August 04, 2017 Published: August 24, 2017
Although the long noncoding RNA AFAP1-AS1 has been shown to be involved in various types of cancer, its involvement in lung cancer remains poorly understood. In the current study, we found that AFAP1-AS1 was substantially over expressed in lung cancer tissues and cell lines. In addition, AFAP1-AS1 expression level was proven to be associated with the malignant features of lung cancer. Knockdown of AFAP1-AS1 significantly suppressed cell proliferation by increasing cell apoptosis and G0/G1 phase retardation of cell cycle in lung cancer cells. Furthermore, AFAP1-AS1 knockdown could suppress tumor growth of lung cancer in BALB/c nude mice. We also identified that AFAP1-AS1 silencing could influence the expression of AFAP1 and KRT1 on mRNA and protein level by cis and trans regulatory mechanism. Moreover, the oncogenic activities of AFAP1-AS1 on cell proliferation are partially mediated by KRT1. In summary, these findings demonstrate that AFAP1-AS1 plays an essential role in promoting lung cancer development in vitro and vivo. It indicated that AFAP1-AS1 is a promising prognostic predictor for patients with lung cancer.
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