D-P Li1, W Chai, Y-H Liu, T-T Xu, H Huang. 1. Department of Otorhinolaryngology Head and Neck Surgery, The People's Hospital of Bozhou; Bozhou Clinical Medicine College of Anhui Medical University; Affiliated Bozhou Hospital of Anhui University of Science and Technology, Bozhou, China.
Abstract
OBJECTIVE: To elucidate whether microRNA-142 could regulate the development of nasopharyngeal carcinoma (NPC) by mediating gene of phosphate and tension homology deleted on chromosome ten (PTEN) expression. PATIENTS AND METHODS: The microRNA-142 expression in NPC tissues and paracancerous tissues was detected by the quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Correlation between the microRNA-142 expression and the prognosis of NPC patients was analyzed. MicroRNA-142 expression in NPC cell lines was determined as well. By transfection of microRNA-142 inhibitor or negative control, biological performances of NPC cells were accessed through cell counting kit-8 (CCK-8), colony formation, wound healing, and transwell assay. Dual-luciferase reporter gene assay was conducted to verify the binding condition between microRNA-142 and its target gene PTEN. Rescue experiments were carried out by co-transfection of microRNA-142 inhibitor and si-PTEN, followed by detecting the invasive capacity of NPC cells. Protein expressions of relative genes in the PI3K/AKT pathway after the microRNA-142 knockdown in NPC cells were determined by Western blot. RESULTS: MicroRNA-142 was highly expressed in NPC tissues than that of paracancerous tissues, which was correlated with poor prognosis of NPC patients. MicroRNA-142 was also highly expressed in NPC cells. Downregulated microRNA-142 inhibited proliferative, migratory, and invasive capacities of NPC cells. Dual-luciferase reporter gene assay verified that microRNA-142 could directly bind to PTEN. Knockdown of PTEN could reverse the inhibitory effect of microRNA-142 on invasive capacity of NPC cells. Finally, Western blot results demonstrated that the microRNA-142 knockdown inhibited the PI3K/AKT pathway in NPC cells. CONCLUSIONS: MicroRNA-142 is highly expressed in NPC. MicroRNA-142 enhances the proliferative and invasive capacities of NPC cells by inhibiting PTEN expression, thus promoting NPC development.
OBJECTIVE: To elucidate whether microRNA-142 could regulate the development of nasopharyngeal carcinoma (NPC) by mediating gene of phosphate and tension homology deleted on chromosome ten (PTEN) expression. PATIENTS AND METHODS: The microRNA-142 expression in NPC tissues and paracancerous tissues was detected by the quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Correlation between the microRNA-142 expression and the prognosis of NPC patients was analyzed. MicroRNA-142 expression in NPC cell lines was determined as well. By transfection of microRNA-142 inhibitor or negative control, biological performances of NPC cells were accessed through cell counting kit-8 (CCK-8), colony formation, wound healing, and transwell assay. Dual-luciferase reporter gene assay was conducted to verify the binding condition between microRNA-142 and its target gene PTEN. Rescue experiments were carried out by co-transfection of microRNA-142 inhibitor and si-PTEN, followed by detecting the invasive capacity of NPC cells. Protein expressions of relative genes in the PI3K/AKT pathway after the microRNA-142 knockdown in NPC cells were determined by Western blot. RESULTS: MicroRNA-142 was highly expressed in NPC tissues than that of paracancerous tissues, which was correlated with poor prognosis of NPC patients. MicroRNA-142 was also highly expressed in NPC cells. Downregulated microRNA-142 inhibited proliferative, migratory, and invasive capacities of NPC cells. Dual-luciferase reporter gene assay verified that microRNA-142 could directly bind to PTEN. Knockdown of PTEN could reverse the inhibitory effect of microRNA-142 on invasive capacity of NPC cells. Finally, Western blot results demonstrated that the microRNA-142 knockdown inhibited the PI3K/AKT pathway in NPC cells. CONCLUSIONS: MicroRNA-142 is highly expressed in NPC. MicroRNA-142 enhances the proliferative and invasive capacities of NPC cells by inhibiting PTEN expression, thus promoting NPC development.