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3-Phosphoinositide Dependent Protein Kinase-1 (PDK-1) Promotes Migration and Invasion in Gastric Cancer Cells Through Activating the NF-κB Pathway
Gastric cancer (GC) is one of the most common cancers and the second leading cause of cancer deaths in the world. Many factors have been reported regarding the progression and development of GC. In this study, we aimed to investigate the correlation of 3-phosphoinositide dependent protein kinase-1 (...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Cognizant Communication Corporation
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7841078/ https://www.ncbi.nlm.nih.gov/pubmed/28109078 http://dx.doi.org/10.3727/096504017X14845839228545 |
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author | Wu, Ning He, Changyu Zhu, Bohui Jiang, Jinling Chen, Yiwen Ma, Tao |
author_facet | Wu, Ning He, Changyu Zhu, Bohui Jiang, Jinling Chen, Yiwen Ma, Tao |
author_sort | Wu, Ning |
collection | PubMed |
description | Gastric cancer (GC) is one of the most common cancers and the second leading cause of cancer deaths in the world. Many factors have been reported regarding the progression and development of GC. In this study, we aimed to investigate the correlation of 3-phosphoinositide dependent protein kinase-1 (PDK-1) with cell viability, migration, and invasion of GC. The expression of PDK-1 was measured in different GC cell lines. Thereafter, the expression of PDK-1 was interfered by small hairpin RNA (shRNA) and then incubated with or without the inhibitor of nuclear factor-κB (NF-κB) pyrrolidine dithiocarbamate (PDTC). We then investigated the effects of PDK-1 aberrant expression on GC cell viability, migration, invasion, and the epithelial–mesenchymal transition (EMT) progress. The results showed that PDK-1 was highly expressed in GC cells, and PDK-1 promoted cell viability, migration, invasion, and EMT in GC. Moreover, we confirmed that PDK-1 activated the phosphatidylinositol 3-hydroxy kinase (PI3K)/AKT and NF-κB signaling pathways. However, administration of PDTC reversed the effects of overexpression of PDK-1 on cell migration and invasion. All these findings suggest that PDK-1 may be involved in progression of GC and could be a new therapeutic target for this disease. |
format | Online Article Text |
id | pubmed-7841078 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Cognizant Communication Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-78410782021-02-16 3-Phosphoinositide Dependent Protein Kinase-1 (PDK-1) Promotes Migration and Invasion in Gastric Cancer Cells Through Activating the NF-κB Pathway Wu, Ning He, Changyu Zhu, Bohui Jiang, Jinling Chen, Yiwen Ma, Tao Oncol Res Article Gastric cancer (GC) is one of the most common cancers and the second leading cause of cancer deaths in the world. Many factors have been reported regarding the progression and development of GC. In this study, we aimed to investigate the correlation of 3-phosphoinositide dependent protein kinase-1 (PDK-1) with cell viability, migration, and invasion of GC. The expression of PDK-1 was measured in different GC cell lines. Thereafter, the expression of PDK-1 was interfered by small hairpin RNA (shRNA) and then incubated with or without the inhibitor of nuclear factor-κB (NF-κB) pyrrolidine dithiocarbamate (PDTC). We then investigated the effects of PDK-1 aberrant expression on GC cell viability, migration, invasion, and the epithelial–mesenchymal transition (EMT) progress. The results showed that PDK-1 was highly expressed in GC cells, and PDK-1 promoted cell viability, migration, invasion, and EMT in GC. Moreover, we confirmed that PDK-1 activated the phosphatidylinositol 3-hydroxy kinase (PI3K)/AKT and NF-κB signaling pathways. However, administration of PDTC reversed the effects of overexpression of PDK-1 on cell migration and invasion. All these findings suggest that PDK-1 may be involved in progression of GC and could be a new therapeutic target for this disease. Cognizant Communication Corporation 2017-08-07 /pmc/articles/PMC7841078/ /pubmed/28109078 http://dx.doi.org/10.3727/096504017X14845839228545 Text en Copyright © 2017 Cognizant, LLC. http://creativecommons.org/licenses/by-nc-nd/4.0/ This article is licensed under a Creative Commons Attribution-NonCommercial NoDerivatives 4.0 International License. |
spellingShingle | Article Wu, Ning He, Changyu Zhu, Bohui Jiang, Jinling Chen, Yiwen Ma, Tao 3-Phosphoinositide Dependent Protein Kinase-1 (PDK-1) Promotes Migration and Invasion in Gastric Cancer Cells Through Activating the NF-κB Pathway |
title | 3-Phosphoinositide Dependent Protein Kinase-1 (PDK-1) Promotes Migration and Invasion in Gastric Cancer Cells Through Activating the NF-κB Pathway |
title_full | 3-Phosphoinositide Dependent Protein Kinase-1 (PDK-1) Promotes Migration and Invasion in Gastric Cancer Cells Through Activating the NF-κB Pathway |
title_fullStr | 3-Phosphoinositide Dependent Protein Kinase-1 (PDK-1) Promotes Migration and Invasion in Gastric Cancer Cells Through Activating the NF-κB Pathway |
title_full_unstemmed | 3-Phosphoinositide Dependent Protein Kinase-1 (PDK-1) Promotes Migration and Invasion in Gastric Cancer Cells Through Activating the NF-κB Pathway |
title_short | 3-Phosphoinositide Dependent Protein Kinase-1 (PDK-1) Promotes Migration and Invasion in Gastric Cancer Cells Through Activating the NF-κB Pathway |
title_sort | 3-phosphoinositide dependent protein kinase-1 (pdk-1) promotes migration and invasion in gastric cancer cells through activating the nf-κb pathway |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7841078/ https://www.ncbi.nlm.nih.gov/pubmed/28109078 http://dx.doi.org/10.3727/096504017X14845839228545 |
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