N Zhou1, H-L Yan. 1. Department of Respiratory Medicine, Dongying People's Hospital, Dongying, China. yanhouling@.163.com.
Abstract
OBJECTIVE: To explore the role of microRNA-24 (miR-24) in the proliferation and apoptosis of lung carcinoma, and to investigate its underlying mechanism. PATIENTS AND METHODS: The expression level of miR-24 in 50 pairs of lung carcinoma tissues and para-cancerous tissues was detected by quantitative Real-time polymerase chain reaction (qRT-PCR). The relationship between miR-24 expression and pathological indicators of lung carcinoma was analyzed. Meanwhile, the corresponding plasmids of miR-24 were constructed. The viability, proliferation, apoptosis and cell cycle of lung carcinoma cells after transfection with miR-24 plasmids were detected by cell counting kit-8 (CCK-8), colony formation assay, and flow cytometry, respectively. The binding condition of miR-24 and MAPK7 was predicted by bioinformatics and verified by Luciferase reporter gene assay. The regulatory effect of miR-24 on MAPK7 in lung carcinoma cells was further detected. RESULTS: MiR-24 was significantly overexpressed in lung carcinoma tissues than that of para-cancerous tissues. Compared with lung carcinoma patients with Grade I-II and tumor size smaller than 3 cm, upregulated miR-24 expression was observed in those with Grade III-IV and tumor size larger than 3 cm. The overall survival (OS) of patients with higher miR-24 expression was remarkably shorter than those with lower expression. Results of clinical data analysis suggested that miR-24 expression was correlated with tumor size and tumor node metastasis (TNM), whereas not correlated with age, gender and lymph node metastasis. In vitro experiments demonstrated that miR-24 overexpression promoted the viability, proliferation and cell cycle of lung carcinoma cells, whereas inhibited cell apoptosis. Furthermore, luciferase reporter gene assay indicated that miR-24 could bind to MAPK7. Meanwhile, overexpressed miR-24 resulted in decreased mRNA and protein levels of MAPK7. In addition, decreased apoptosis and increased cell cycle induced by miR-24 overexpression could be partially reversed by MAPK7 overexpression. CONCLUSIONS: We found that miR-24 promoted lung carcinoma development by increasing cell proliferation and inhibiting cell apoptosis via targeting MAPK7.
OBJECTIVE: To explore the role of microRNA-24 (miR-24) in the proliferation and apoptosis of lung carcinoma, and to investigate its underlying mechanism. PATIENTS AND METHODS: The expression level of miR-24 in 50 pairs of lung carcinoma tissues and para-cancerous tissues was detected by quantitative Real-time polymerase chain reaction (qRT-PCR). The relationship between miR-24 expression and pathological indicators of lung carcinoma was analyzed. Meanwhile, the corresponding plasmids of miR-24 were constructed. The viability, proliferation, apoptosis and cell cycle of lung carcinoma cells after transfection with miR-24 plasmids were detected by cell counting kit-8 (CCK-8), colony formation assay, and flow cytometry, respectively. The binding condition of miR-24 and MAPK7 was predicted by bioinformatics and verified by Luciferase reporter gene assay. The regulatory effect of miR-24 on MAPK7 in lung carcinoma cells was further detected. RESULTS:MiR-24 was significantly overexpressed in lung carcinoma tissues than that of para-cancerous tissues. Compared with lung carcinomapatients with Grade I-II and tumor size smaller than 3 cm, upregulated miR-24 expression was observed in those with Grade III-IV and tumor size larger than 3 cm. The overall survival (OS) of patients with higher miR-24 expression was remarkably shorter than those with lower expression. Results of clinical data analysis suggested that miR-24 expression was correlated with tumor size and tumor node metastasis (TNM), whereas not correlated with age, gender and lymph node metastasis. In vitro experiments demonstrated that miR-24 overexpression promoted the viability, proliferation and cell cycle of lung carcinoma cells, whereas inhibited cell apoptosis. Furthermore, luciferase reporter gene assay indicated that miR-24 could bind to MAPK7. Meanwhile, overexpressed miR-24 resulted in decreased mRNA and protein levels of MAPK7. In addition, decreased apoptosis and increased cell cycle induced by miR-24 overexpression could be partially reversed by MAPK7 overexpression. CONCLUSIONS: We found that miR-24 promoted lung carcinoma development by increasing cell proliferation and inhibiting cell apoptosis via targeting MAPK7.