RESUMO
The aim of this study was to probe the influence of microRNA-301b (miR-301b) in esophageal cancer pathogenesis. Based on the data acquired from The Cancer Genome Atlas database, we found that miR-301b was highly expressed in esophageal cancer tissues and high expression of miR-301b was related to worse prognosis in patients with esophageal cancer. Quantitative real-time PCR revealed that the expression of miR-301b was higher in all examined esophageal cancer cell lines (ECA109, KY-SE150, TE-1, and NEC) than that in a human esophageal epithelial cell line (HEEC). Upregulation/downregulation of miR-301b facilitated/suppressed the growth, migration, and invasion of ECA109/KY-SE150 cells. Synaptosome-associated protein 91 (SNAP91) was proved to be one of the target genes of miR-301b and was negatively modulated by miR-301b. Besides, SNAP91 was lowly expressed in human esophageal cancer tissues and cell lines. Meanwhile, low expression of SNAP91 was concerned with poor prognosis in patients with esophageal cancer. Furthermore, we discovered that overexpression/depletion of SNAP91 suppressed/facilitated the proliferation of KY-SE150/ECA109 cells. MiR-301b and SNAP91 had little impact on HEEC cell proliferation and this degree of influence was negligible compared with their impacts on esophageal cancer cell proliferation. By rescue assay, we showed that overexpression of SNAP91 restrained the growth, migration, and invasion of ECA109 cells with overexpressed miR-301b while knockdown of SNAP91 showed the contrary effects on KY-SE150 cells with downregulated miR-301b. These consequences indicated that miR-301b played an important effect on esophageal cancer cells through regulating SNAP91, insinuating that miR-301b/SNAP91 might be novel potential targets for esophageal cancer therapy and prognosis.
Assuntos
Biomarcadores Tumorais/metabolismo , Neoplasias Esofágicas/patologia , Carcinoma de Células Escamosas do Esôfago/patologia , Regulação Neoplásica da Expressão Gênica , MicroRNAs/genética , Proteínas Monoméricas de Montagem de Clatrina/metabolismo , Apoptose , Biomarcadores Tumorais/genética , Proliferação de Células , Neoplasias Esofágicas/genética , Neoplasias Esofágicas/metabolismo , Carcinoma de Células Escamosas do Esôfago/genética , Carcinoma de Células Escamosas do Esôfago/metabolismo , Feminino , Humanos , Masculino , Proteínas Monoméricas de Montagem de Clatrina/genética , Prognóstico , Taxa de Sobrevida , Células Tumorais CultivadasRESUMO
We assessed the expression of Serpin Family E Member 1 (SERPINE1) and its prognostic values in gastric adenocarcinoma (GAC) by using the data from TCGA database. The biological functions of SERPINE1 in GAC cells were detected by cell counting Kit-8, colony-forming, Transwell, and wound-healing assays, appropriately. Relative mRNA and protein levels were detected by RT-qPCR and western blot. Bioinformatics analysis indicated that SERPINE1 was significantly up-regulated in GAC tissues compared to normal tissues. High SERPINE1 expression led to a short overall survival and could act as an independent prognosticator for GAC patients. Besides, down-regulation of SERPINE1 showed a suppressive effect on the phenotype of GAC cells and significantly inhibited the EMT process. Over-expression of SERPINE1 got the reverse outcomes. These data suggest that SERPINE1 contributes to the proliferation, invasion and migration of GAC cells, insinuating that SERPINE1 may be considered as a novel biomarker for GAC treatment.
