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Na(+)/H(+) exchanger regulatory factor 1 overexpression suppresses the malignant phenotype of MIAPaCa-2 pancreatic adenocarcinoma cells by downregulating Akt phosphorylation

Na(+)/H(+) exchanger regulatory factor 1 (NHERF1) is reported to be associated with the development of numerous types of tumor; however, its effects on the metastasis of pancreatic adenocarcinoma are not fully understood. In the present study, it was revealed that the expression level of NHERF1 in p...

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Detalles Bibliográficos
Autores principales: Zhang, Xibo, Liu, Junjian, Li, Zhonglian
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5920473/
https://www.ncbi.nlm.nih.gov/pubmed/29725468
http://dx.doi.org/10.3892/ol.2018.8289
Descripción
Sumario:Na(+)/H(+) exchanger regulatory factor 1 (NHERF1) is reported to be associated with the development of numerous types of tumor; however, its effects on the metastasis of pancreatic adenocarcinoma are not fully understood. In the present study, it was revealed that the expression level of NHERF1 in pancreatic adenocarcinoma is decreased compared with normal pancreatic tissue based on the analysis of a protein expression database. The present study was undertaken in order to investigate the potential effects of NHERF1 overexpression on the malignant phenotype of MIAPaCa-2 pancreatic adenocarcinoma cells. NHERF1 was stably overexpressed in this cell line, and Cell Counting Kit-8, wound healing and Transwell assays were used to detect the proliferative and migratory abilities of the cells. NHERF1 overexpression suppressed proliferation in the MIAPaCa-2 cell line compared with empty vector-transfected (negative control) cells. Additionally, NHERF1 overexpression significantly inhibited the migration of MIAPaCa-2 cells. The results of a western blot analysis identified that NHERF1 overexpression markedly decreased the expression of phosphorylated-protein kinase B (p-Akt), while no significant difference was observed between untransfected and negative control cells. Taken together, these results suggested that NHERF1 may be able to inhibit the proliferation and migration and alter the malignant phenotype of pancreatic adenocarcinoma cells via reduction of p-Akt levels. These findings indicate a potential novel approach to the treatment of pancreatic adenocarcinoma.