Weiguo Ma1, Xin Zhao2, Ning Xue1, Yun Gao1, Qingxia Xu1. 1. Department of Clinical Laboratory, the Affiliated Cancer Hospital of Zhengzhou University, Henan Cancer Hospital, Zhengzhou, China. 2. Department of Clinical Laboratory, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Abstract
PURPOSE: It is generally accepted that long noncoding RNAs (lncRNAs) function as vital regulators of tumor development and progression. Long intergenic non-coding RNA 1410 (LINC01410) is a newly discovered lncRNA, and its role in osteosarcoma (OS) is yet to be determined. MATERIALS AND METHODS: The expression of LINC01410, microRNA-122-5p (miR-122-5p), and N-myc downstream-regulated gene 3 (NDRG3) in OS tissues was determined using reverse transcription-quantitative PCR. Interactions between LINC01410, miR-122-5p, and NDRG3 were predicted and verified using bioinformatics tools and luciferase assays. Cell proliferation, migration, and invasion were detected using cell counting Kit-8 and Transwell assays. RESULTS: LINC01410 was overexpressed in OS tissues. Furthermore, it was confirmed that LINC01410 facilitated OS cell proliferation and migration. Our studies also showed that LINC01410 binds to miR-122-5p, and miR-122-5p binds to NDRG3. Finally, we observed that LINC01410 knockdown inhibited the proliferation, invasion, and migration of OS cells. Knockdown of LINC01410 resulted in the upregulation of miR-122-5p and downregulation of NDRG3. CONCLUSION: Our results demonstrated that the LINC01410/miR-122-5p/NDRG3 axis is involved in the progression of OS.
PURPOSE: It is generally accepted that long noncoding RNAs (lncRNAs) function as vital regulators of tumor development and progression. Long intergenic non-coding RNA 1410 (LINC01410) is a newly discovered lncRNA, and its role in osteosarcoma (OS) is yet to be determined. MATERIALS AND METHODS: The expression of LINC01410, microRNA-122-5p (miR-122-5p), and N-myc downstream-regulated gene 3 (NDRG3) in OS tissues was determined using reverse transcription-quantitative PCR. Interactions between LINC01410, miR-122-5p, and NDRG3 were predicted and verified using bioinformatics tools and luciferase assays. Cell proliferation, migration, and invasion were detected using cell counting Kit-8 and Transwell assays. RESULTS: LINC01410 was overexpressed in OS tissues. Furthermore, it was confirmed that LINC01410 facilitated OS cell proliferation and migration. Our studies also showed that LINC01410 binds to miR-122-5p, and miR-122-5p binds to NDRG3. Finally, we observed that LINC01410 knockdown inhibited the proliferation, invasion, and migration of OS cells. Knockdown of LINC01410 resulted in the upregulation of miR-122-5p and downregulation of NDRG3. CONCLUSION: Our results demonstrated that the LINC01410/miR-122-5p/NDRG3 axis is involved in the progression of OS.