OBJECTIVE: To explore the role of microRNA-203 in laryngeal cancer and its underlying mechanism in regulating cell invasion and apoptosis. PATIENTS AND METHODS: MicroRNA-203 expression in laryngeal cancer tissues and paracancerous tissues was detected by quantitative real time-polymerase chain reaction (qRT-PCR). The regulatory effects of microRNA-203 on the invasion and apoptosis of laryngeal cancer cells were detected by transwell assay and flow cytometry, respectively. Dual-Luciferase reporter gene assay was performed to access the binding condition of microRNA-203 and LASP1. Both mRNA and protein levels of LASP1 in laryngeal cancer cells were detected after transfection with microRNA-203 mimic or microRNA-203 inhibitor by qRT-PCR and Western blot, respectively. Rescue experiments were finally performed to detect whether microRNA-203 regulates laryngeal cancer development via targeting LASP1. RESULTS: MicroRNA-203 was lowly expressed in laryngeal cancer tissues and cell lines. MicroRNA-203 knockdown in Hep-2 cells can promote the invasion and inhibit the apoptosis of laryngeal cancer cells. Subsequently, LASP1 was predicted to be the target gene of microRNA-203, which was further verified by the Dual-Luciferase reporter gene assay. LASP1 expression was negatively regulated by microRNA-203. Furthermore, rescue experiments showed that the regulatory effects of microRNA-203 on the invasion and apoptosis of laryngeal cancer cells were reversed by LASP1. CONCLUSIONS: We showed that lowly expressed microRNA-203 could promote the invasion and inhibit apoptosis of laryngeal cancer cells via inhibiting LASP1.
OBJECTIVE: To explore the role of microRNA-203 in laryngeal cancer and its underlying mechanism in regulating cell invasion and apoptosis. PATIENTS AND METHODS: MicroRNA-203 expression in laryngeal cancer tissues and paracancerous tissues was detected by quantitative real time-polymerase chain reaction (qRT-PCR). The regulatory effects of microRNA-203 on the invasion and apoptosis of laryngeal cancer cells were detected by transwell assay and flow cytometry, respectively. Dual-Luciferase reporter gene assay was performed to access the binding condition of microRNA-203 and LASP1. Both mRNA and protein levels of LASP1 in laryngeal cancer cells were detected after transfection with microRNA-203 mimic or microRNA-203 inhibitor by qRT-PCR and Western blot, respectively. Rescue experiments were finally performed to detect whether microRNA-203 regulates laryngeal cancer development via targeting LASP1. RESULTS: MicroRNA-203 was lowly expressed in laryngeal cancer tissues and cell lines. MicroRNA-203 knockdown in Hep-2 cells can promote the invasion and inhibit the apoptosis of laryngeal cancer cells. Subsequently, LASP1 was predicted to be the target gene of microRNA-203, which was further verified by the Dual-Luciferase reporter gene assay. LASP1 expression was negatively regulated by microRNA-203. Furthermore, rescue experiments showed that the regulatory effects of microRNA-203 on the invasion and apoptosis of laryngeal cancer cells were reversed by LASP1. CONCLUSIONS: We showed that lowly expressed microRNA-203 could promote the invasion and inhibit apoptosis of laryngeal cancer cells via inhibiting LASP1.