H-B Lu1. 1. Department of Radiotherapy, Jiangsu Province Danyang People's Hospital, Danyang, China. 634422921@qq.com.
Abstract
OBJECTIVE: To detect the expression of microRNA-556-3p in esophageal cancer (EC) tissues and to elucidate the mechanisms underlying microRNA-556-3p in promoting EC progression. PATIENTS AND METHODS: QRT-PCR (quantitative Real-Time Polymerase Chain Reaction) was performed to detect microRNA-556-3p expression in 65 cases of EC tissues, 30 cases of normal esophageal tissues and EC cell lines. The overall survival (OS) of EC patients was calculated based on the 10-year follow-up data. For in vitro experiments, MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) and transwell assay were performed to evaluate the effect of microRNA-556-3p on the proliferative and invasive abilities of EC cells. The effect of microRNA-556-3p on DAB2IP and MAPK pathway was determined by Western blot and qRT-PCR. The binding condition between microRNA-556-3p and DAB2IP was further confirmed by Luciferase reporter gene assay. RESULTS: MicroRNA-556-3p expression was upregulated in EC tissues than that of paracancerous tissues. EC patients with higher expression of microRNA-556-3p presented a shorter OS than those with lower expression. Moreover, microRNA-556-3p overexpression in EC cells remarkably promoted cell viability. Upregulated microRNA-556-3p in Eca109 and Eca7906 cell lines markedly increased cell proliferation and invasion. The expression level of DAB2IP was negatively regulated by microRNA-556-3p verified by the Luciferase reporter gene assay. CONCLUSIONS: MicroRNA-556-3p blocked the translation of DAB2IP at mRNA level by directly binding to 3'UTR of DAB2IP, thereafter enhancing the proliferation of Eca109 and Eca7906 cells. MicroRNA-556-3p promoted the occurrence and development of EC. Our study provided a new theoretical basis and therapeutic target for EC treatment.
OBJECTIVE: To detect the expression of microRNA-556-3p in esophageal cancer (EC) tissues and to elucidate the mechanisms underlying microRNA-556-3p in promoting EC progression. PATIENTS AND METHODS: QRT-PCR (quantitative Real-Time Polymerase Chain Reaction) was performed to detect microRNA-556-3p expression in 65 cases of EC tissues, 30 cases of normal esophageal tissues and EC cell lines. The overall survival (OS) of EC patients was calculated based on the 10-year follow-up data. For in vitro experiments, MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) and transwell assay were performed to evaluate the effect of microRNA-556-3p on the proliferative and invasive abilities of EC cells. The effect of microRNA-556-3p on DAB2IP and MAPK pathway was determined by Western blot and qRT-PCR. The binding condition between microRNA-556-3p and DAB2IP was further confirmed by Luciferase reporter gene assay. RESULTS: MicroRNA-556-3p expression was upregulated in EC tissues than that of paracancerous tissues. EC patients with higher expression of microRNA-556-3p presented a shorter OS than those with lower expression. Moreover, microRNA-556-3p overexpression in EC cells remarkably promoted cell viability. Upregulated microRNA-556-3p in Eca109 and Eca7906 cell lines markedly increased cell proliferation and invasion. The expression level of DAB2IP was negatively regulated by microRNA-556-3p verified by the Luciferase reporter gene assay. CONCLUSIONS: MicroRNA-556-3p blocked the translation of DAB2IP at mRNA level by directly binding to 3'UTR of DAB2IP, thereafter enhancing the proliferation of Eca109 and Eca7906 cells. MicroRNA-556-3p promoted the occurrence and development of EC. Our study provided a new theoretical basis and therapeutic target for EC treatment.