BACKGROUND: Long noncoding RNAs (lncRNAs) play essential roles in tumor progression. Aberrant colorectal cancer-associated lncRNA (CCAL) has been found in colorectal cancer. However, the function of lncRNA CCAL in osteosarcoma (OS) remains unclear. METHODS: Quantitative real-time PCR (qRT-PCR) was performed to measure CCAL expression in OS tissues and adjacent nontumor tissues. The correlation betweent CCAL expression and clinicopathological features and prognosis was also analyzed. In addition, the function of CCAL was further evaluated by cell proliferation, migration and invasion assays. RESULTS: We showed that CCAL was significantly up-regulated in OS tissues compared with adjacent nontumor tissues. Increased expression of CCAL was correlated with advanced TNM stage and metastasis. Kaplan-Meier analysis demonstrated that patients with high CCAL expression had lower overall survival than those with low CCAL expression. Multivariate Cox regression analysis indicated that CCAL expression might be an independent prognostic factor for OS patients. In addition, functional assays showed that decreased CCAL expression could inhibit OS cell proliferation, migration and invasion ability. CONCLUSIONS: Our findings suggested that CCAL plays critical roles in OS progression and could act as a therapeutic target in the treatment of OS.
BACKGROUND: Long noncoding RNAs (lncRNAs) play essential roles in tumor progression. Aberrant colorectal cancer-associated lncRNA (CCAL) has been found in colorectal cancer. However, the function of lncRNA CCAL in osteosarcoma (OS) remains unclear. METHODS: Quantitative real-time PCR (qRT-PCR) was performed to measure CCAL expression in OS tissues and adjacent nontumor tissues. The correlation betweent CCAL expression and clinicopathological features and prognosis was also analyzed. In addition, the function of CCAL was further evaluated by cell proliferation, migration and invasion assays. RESULTS: We showed that CCAL was significantly up-regulated in OS tissues compared with adjacent nontumor tissues. Increased expression of CCAL was correlated with advanced TNM stage and metastasis. Kaplan-Meier analysis demonstrated that patients with high CCAL expression had lower overall survival than those with low CCAL expression. Multivariate Cox regression analysis indicated that CCAL expression might be an independent prognostic factor for OS patients. In addition, functional assays showed that decreased CCAL expression could inhibit OS cell proliferation, migration and invasion ability. CONCLUSIONS: Our findings suggested that CCAL plays critical roles in OS progression and could act as a therapeutic target in the treatment of OS.