High Expression of lncRNA AFAP1-AS1 Promotes the Progression of Colon Cancer and Predicts Poor Prognosis
Hao Boa b c, Liqing Fana, Jingjing Lid, Zhizhong Liue, Shanshan Zhangc, Lei Shib, Can Jie Guob, Xiayu Lib c d, Qianjin Liaob e, Wenling Zhangb, Ming Zhoub c, Bo Xiangb c,
- aInstitute of Reproductive and Stem Cell Engineering, School of Basic Medical Science, Central South University, Changsha, China
- bThe Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Cancer Research Institute and School of Basic Medical Sciences, Central South University, Changsha, Hunan, China
- cThe Key Laboratory of Carcinogenesis of the Chinese Ministry of Health, Xiangya Hospital, Central South University, Changsha, Hunan, China
- dDepartment of Plastic Surgery, Hunan Key Laboratory of Nonresolving Inflammation and Cancer, Disease Genome Research Center, Third Xiangya Hospital, Central South University, Changsha, China
- eHunan Key Laboratory of Translational Radiation Oncology, Hunan Cancer Hospital and The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, China
- fDepartment of Oral and Maxillofacial Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China
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Abstract
Long non-coding RNAs (lncRNAs) are dysregulated in various cancers.However, the clinical relevance and functional roles of AFAP1-AS1 in colon cancer (CC) have not been clarified.We analyzed the lncRNA expression patterns in Gene Expression Omnibus (GEO) datasets and the Cancer Genome Atlas (TCGA) RNA-seq datasets, and found that the expression level of AFAP1-AS1 was significantly elevated in CC tissues.High levels of AFAP1-AS1 were associated with poor disease-free survival and overall survival in CC patients.In vitro experiments demonstrated that AFAP1-AS1 knockdown significantly inhibited the cell invasive and migration capability in CC cell line HT-29.AFAP1-AS1 knockdown also increased the expression of E-cadherin and ZO-1 while inhibited the expression of Vimentin, MMP9, ZEB1 and β-catenin, suggesting that AFAP1-AS1 is involved in the epithelial-mesenchymal transition (EMT) process of CC.Further studies confirmed that AFAP1-AS1 knockdown also affected the actin-cytokeratin signaling pathway.Thus, AFAP1-AS1 might be a potential novel diagnostic marker and therapeutic target for CC.
TL;DRAnalysis of lncRNA expression patterns in Gene Expression Omnibus and Cancer Genome Atlas datasets found that high levels of AFAP1-AS1 were associated with poor disease-free survival and overall survival in CC patients and might be a potential novel diagnostic marker and therapeutic target for CC. (Semantic Scholar)