Objective: Long non-coding RNAs (lncRNAs) are a new class of noncoding RNAs, which serve as crucial regulators in tumor progression, including osteosarcoma (OS). The objective of this study is to uncover the clinical significance and biological role of lncRNA CDKN2B antisense RNA 1 (CDKN2B-AS1) in OS. Methods: Quantitative real time PCR analysis was used to determine the expression of CDKN2B-AS1 in OS tissues and cell lines. The associations between CDKN2B-AS1 expression and clinicopathological characteristics of OS patients were assessed by Chi-squared test. CCK-8, colony formation, flow cytometry and transwell assay were utilized to evaluate the effects of CDKN2B-AS1 knockdown on cell proliferation, cell cycle, migration and invasion. The protein expression associated with cell cycle and epithelial-mesenchymal transition (EMT) was measured by western blotting. Results: CDKN2B-AS1 was found to be markedly up-regulated in OS tissues and cell lines. Clinical data further demonstrated highly expressed CDKN2B-AS1 tended to be strongly positively correlated with tumor size, distant metastasis and TNM stage. Loss-of-function of CDKN2B-AS1 leaded to inhibited cell proliferation and induced cell cycle G0/G1 phase arrest. In addition, CDKN2B-AS1 knockdown significantly suppressed OS cells migration and invasion. Mechanistically, CDKN2B-AS1 knockdown in OS cells suppressed the expression of CDK4 and Cyclin D1, as well as EMT, as demonstrated by elevated levels of epithelial markers (E-cadherin) and downregulation of mesenchymal markers (vimentin and N-cadherin). Conclusions: Taken together, our findings suggest that CDKN2B-AS1 represents a potential therapeutic target for OS.
Objective: Long non-coding RNAs (lncRNAs) are a new class of noncoding RNAs, which serve as crucial regulators in tumor progression, including osteosarcoma (OS). The objective of this study is to uncover the clinical significance and biological role of lncRNA CDKN2B antisense RNA 1 (CDKN2B-AS1) in OS. Methods: Quantitative real time PCR analysis was used to determine the expression of CDKN2B-AS1 in OS tissues and cell lines. The associations between CDKN2B-AS1 expression and clinicopathological characteristics of OS patients were assessed by Chi-squared test. CCK-8, colony formation, flow cytometry and transwell assay were utilized to evaluate the effects of CDKN2B-AS1 knockdown on cell proliferation, cell cycle, migration and invasion. The protein expression associated with cell cycle and epithelial-mesenchymal transition (EMT) was measured by western blotting. Results:CDKN2B-AS1 was found to be markedly up-regulated in OS tissues and cell lines. Clinical data further demonstrated highly expressed CDKN2B-AS1 tended to be strongly positively correlated with tumor size, distant metastasis and TNM stage. Loss-of-function of CDKN2B-AS1 leaded to inhibited cell proliferation and induced cell cycle G0/G1 phase arrest. In addition, CDKN2B-AS1 knockdown significantly suppressed OS cells migration and invasion. Mechanistically, CDKN2B-AS1 knockdown in OS cells suppressed the expression of CDK4 and Cyclin D1, as well as EMT, as demonstrated by elevated levels of epithelial markers (E-cadherin) and downregulation of mesenchymal markers (vimentin and N-cadherin). Conclusions: Taken together, our findings suggest that CDKN2B-AS1 represents a potential therapeutic target for OS.