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Abstract
Osteosarcoma (OS) is a kind of fatal primary bone tumors in adolescents and young adults. Long noncoding RNAs (lncRNAs) are a group of noncoding RNAs which occupy a part of the latest hot topics. We aimed to investigate the roles of lncRNA LINC00665 in OS in this study. In this study, we found that LINC00665 was highly expressed in OS tissues and cell lines, and its high expression was associated with malignant feature and poor prognosis of OS. In OS cells, LINC00665 could facilitate the proliferation, migration, and invasion to play an oncogenic role. Mechanistically, LINC00665 served as a sponge for miR-708 and miR-142-5p and positively mediated the expression of their target RAP1B. Finally, we confirmed that LINC00665 exercised its biological functions by mediating RAP1B. In conclusion, LINC00665 is overexpressed in OS and facilitates the malignant processes of OS cells by increasing the RAP1B expression via sponging miR-708 and miR-142-5p.
Highlights
Osteosarcoma (OS) is one of the most frequently occurring primary bone tumors in adolescents and young adults [1, 2]
LncRNA CEBPA-AS1 is found to be weakly expressed in OS and inhibit proliferation and migration and stimulate apoptosis of OS cells [11]
LncRNA RP11-361F15.2 is significantly increased in OS and promotes osteosarcoma tumorigenesis by inhibiting M2-Like polarization of tumor-associated macrophages of CPEB4 [12]
Summary
Osteosarcoma (OS) is one of the most frequently occurring primary bone tumors in adolescents and young adults [1, 2]. Long noncoding RNAs (lncRNAs) are a group of noncoding RNAs with over 200 nucleotides in length and have no protein-coding ability [5]. They are involved in a wide array of physiological and biological cellular processes including transcriptional regulation, epigenetic modification, and acting as microRNA (miRNA) sponges [6,7,8]. A large number of lncRNAs have been found to be abnormally expressed in multiple tumors, exerting great impacts on carcinogenesis and cancer progression [9]. LncRNA RP11-361F15.2 is significantly increased in OS and promotes osteosarcoma tumorigenesis by inhibiting M2-Like polarization of tumor-associated macrophages of CPEB4 [12]
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