Affiliations: [a] Department of Geriatrics, The Sixth Hospital of Wuhan, Affiliated Hospital of Jianghan University, Wuhan, Hubei, China | [b] Department of Cardiovascular Medicine, Wuhan Asia Heart Hospital, Wuhan, Hubei, China
Correspondence:
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Corresponding author: Shifang Qu, Department of Geriatrics, The Sixth Hospital of Wuhan, Affiliated Hospital of Jianghan University, No. 168 Hongkong Road, Jiang’an District, Wuhan, Hubei 430015, China. Tel./Fax: +86 15827511588; E-mail: shifangqu7@163.com.
Note: [1] These authors contributed equally to this work.
Abstract: BACKGROUND: Numerous evidence have suggested the vital role of lncRNAs in human tumorigenesis. And lncRNA APAP1-AS1 has been proved to act as an oncogene. OBJECTIVE: Nevertheless, the molecular process underlying ARAP1-AS1 for the lymphoma progression has not been well studied. METHODS: RT-qPCR was used to ascertain the miR-6867-5p and ARAP1-AS1 in lymphoma cells and tissues. The localization of ARAP1-AS1 was determined via subcellular fractionation analysis. A xenograft model was used to investigate the influence of ARAP1-AS1 in formation of tumor in vivo. In addition, interactions between ARAP-AS1 and miR-6867-5p were tested by bioinformatics analysis, RIP assay, luciferase reporter and Pearson’s correlation analysis. Combined with loss-of-function experiments, MTT assays and flow cytometry were performed to evaluate the function of miR-6867-5p and also ARAP-AS1 in proliferation and apoptosis of lymphoma cells, respectively. RESULTS: ARAP1-AS1 was remarkably upregulated in lymphoma cells and tissues, while miR-6867-5p expression was downregulated. Furthermore, high ARAP1-AS1 expression suppressed miR-6867-5p expression in lymphoma cell lines (Raji and CA46), and Pearson’s analysis showed negative correlation between ARAP1-AS1 expression and also miR-6867-5p expression. In addition, knockdown of ARAP1-AS1 resulted in weakened cell viability and uplifted apoptosis rate of lymphoma cells (Raji and CA46) as well as a delay in the tumor growth in vivo. Further investigations illustrated that miR-6867-5p inhibitor reversed all above biological activities. CONCLUSIONS: LncRNA ARAP1-AS1 served as a tumor-promoter in lymphoma cells by sponging with miR-6867-5p, which may help to provide potential therapeutic target gene for lymphoma patients.
