Shian Liao1, Shuxing Xing2, Yanhui Ma3. 1. Department of Bone and Soft Tissue Surgery, Affiliated Tumor Hospital of Guangxi Medical University, Nanning, 530021, Guangxi, China. 2. Department of Orthopedics, Fifth People's Hospital of Chengdu, Chengdu, 611130, Sichuan, China. 3. Department of Orthopedics, Affiliated Hospital, Department Orthoped and Traumatol, Yanan University, No. 43 North Street, Baota District, Yanan, 716000, Shaanxi, China. YanhuiMa_546@163.com.
Abstract
BACKGROUND: As has been illustrated that long noncoding RNAs (lncRNAs) and microRNAs (miRNAs) are potential regulators in the occurrence and progression of human cancers. LncRNA SNHG16 has been identified as an oncogene involved in the progression of human cancers. However, neither the function nor the underlying molecular mechanism of SNHG16 in osteosarcoma has been discovered. PURPOSE: The aim of the study is to explore the role and molecular regulation mechanism of SNHG16 in osteosarcoma. METHODS: The expression of SNHG16 in HNSCC tissues and cells was detected by RT-qPCR assay. The biological function of SNHG16 in osteosarcoma was measured by CCK-8, cell cycle, cell apoptosis and transwell assays. The interaction between SNHG16 and miR-98-5p was studied by luciferase reporter and RIP assays. RESULTS: The ectopic expression of SNHG16 was found in osteosarcoma tissues and cell lines, which indicated poor prognosis and lower overall survival rate of osteosarcoma patients. Knockdown of SNHG16 inhibited cell proliferation, migration, invasion, cell cycle and promoted apoptosis in osteosarcoma. It was demonstrated that SNHG16 directly interacts with miR-98-5p. What's more, we found a significantly negative correlation between SNHG16 and miR-98-5p expression. Finally, rescue experiments revealed that inhibition of miR-98-5p attenuated SNHG16 knockdown-mediated effects on cellular processes in osteosarcoma. CONCLUSIONS: LncRNA SNHG16 regulated cellular processes in osteosarcoma by sponging miR-98-5p, and SNHG16 may be a new and effective molecular therapeutic target for osteosarcoma.
BACKGROUND: As has been illustrated that long noncoding RNAs (lncRNAs) and microRNAs (miRNAs) are potential regulators in the occurrence and progression of humancancers. LncRNA SNHG16 has been identified as an oncogene involved in the progression of humancancers. However, neither the function nor the underlying molecular mechanism of SNHG16 in osteosarcoma has been discovered. PURPOSE: The aim of the study is to explore the role and molecular regulation mechanism of SNHG16 in osteosarcoma. METHODS: The expression of SNHG16 in HNSCC tissues and cells was detected by RT-qPCR assay. The biological function of SNHG16 in osteosarcoma was measured by CCK-8, cell cycle, cell apoptosis and transwell assays. The interaction between SNHG16 and miR-98-5p was studied by luciferase reporter and RIP assays. RESULTS: The ectopic expression of SNHG16 was found in osteosarcoma tissues and cell lines, which indicated poor prognosis and lower overall survival rate of osteosarcomapatients. Knockdown of SNHG16 inhibited cell proliferation, migration, invasion, cell cycle and promoted apoptosis in osteosarcoma. It was demonstrated that SNHG16 directly interacts with miR-98-5p. What's more, we found a significantly negative correlation between SNHG16 and miR-98-5p expression. Finally, rescue experiments revealed that inhibition of miR-98-5p attenuated SNHG16 knockdown-mediated effects on cellular processes in osteosarcoma. CONCLUSIONS: LncRNA SNHG16 regulated cellular processes in osteosarcoma by sponging miR-98-5p, and SNHG16 may be a new and effective molecular therapeutic target for osteosarcoma.