Pleckstrin-2 as a Prognostic Factor and Mediator of Gastric Cancer Progression

Pleckstrin-2 (PLEK2) is a crucial mediator of cytoskeletal reorganization. However, the potential roles of PLEK2 in gastric cancer are still unknown. PLEK2 expression in gastric cancer was examined by western blotting and real-time PCR. Survival analysis was utilized to test the clinical impacts of...

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Main Authors: Jun Wang, Zhigang He, Bo Sun, Wenhai Huang, Jianbin Xiang, Zongyou Chen, Zhenyang Li, Xiaodong Gu
Format: Article
Language:English
Published: Wiley 2021-01-01
Series:Gastroenterology Research and Practice
Online Access:http://dx.doi.org/10.1155/2021/5527387
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author Jun Wang
Zhigang He
Bo Sun
Wenhai Huang
Jianbin Xiang
Zongyou Chen
Zhenyang Li
Xiaodong Gu
author_facet Jun Wang
Zhigang He
Bo Sun
Wenhai Huang
Jianbin Xiang
Zongyou Chen
Zhenyang Li
Xiaodong Gu
author_sort Jun Wang
collection DOAJ
description Pleckstrin-2 (PLEK2) is a crucial mediator of cytoskeletal reorganization. However, the potential roles of PLEK2 in gastric cancer are still unknown. PLEK2 expression in gastric cancer was examined by western blotting and real-time PCR. Survival analysis was utilized to test the clinical impacts of the levels of PLEK2 in gastric cancer patients. In vitro and in vivo studies were used to estimate the potential roles played by PLEK2 in modulating gastric cancer proliferation, self-renewal, and tumourigenicity. Bioinformatics approaches were used to monitor the effect of PLEK2 on epithelial-mesenchymal transition (EMT) signalling pathways. PLEK2 expression was significantly upregulated in gastric cancer as compared with nontumour samples. Kaplan-Meier plotter analysis revealed that gastric cancer patients with higher PLEK2 levels had substantially poorer overall survival compared with gastric cancer patients with lower PLEK2 levels. The upregulation or downregulation of PLEK2 in gastric cancer cell lines effectively enhanced or inhibited cell proliferation and proinvasive behaviour, respectively. Additionally, we also found that PLEK2 enhanced EMT through downregulating E-cadherin expression and upregulating Vimentin expression. Our findings demonstrated that PLEK2 plays a potential role in gastric cancer and may be a novel therapeutic target for gastric cancer.
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spelling doaj-art-e0f96e5f82cb41d6a76369da025c57222025-08-20T02:21:28ZengWileyGastroenterology Research and Practice1687-61211687-630X2021-01-01202110.1155/2021/55273875527387Pleckstrin-2 as a Prognostic Factor and Mediator of Gastric Cancer ProgressionJun Wang0Zhigang He1Bo Sun2Wenhai Huang3Jianbin Xiang4Zongyou Chen5Zhenyang Li6Xiaodong Gu7Department of General Surgery, Huashan Hospital, Fudan University, Shanghai, ChinaDepartment of General Surgery, Shanghai Songjiang District Central Hospital, Shanghai, ChinaDepartment of Gastric Surgery, Fudan University Shanghai Cancer Center, Shanghai, ChinaDepartment of General Surgery, Huashan Hospital, Fudan University, Shanghai, ChinaDepartment of General Surgery, Huashan Hospital, Fudan University, Shanghai, ChinaDepartment of General Surgery, Huashan Hospital, Fudan University, Shanghai, ChinaDepartment of General Surgery, Huashan Hospital, Fudan University, Shanghai, ChinaDepartment of General Surgery, Huashan Hospital, Fudan University, Shanghai, ChinaPleckstrin-2 (PLEK2) is a crucial mediator of cytoskeletal reorganization. However, the potential roles of PLEK2 in gastric cancer are still unknown. PLEK2 expression in gastric cancer was examined by western blotting and real-time PCR. Survival analysis was utilized to test the clinical impacts of the levels of PLEK2 in gastric cancer patients. In vitro and in vivo studies were used to estimate the potential roles played by PLEK2 in modulating gastric cancer proliferation, self-renewal, and tumourigenicity. Bioinformatics approaches were used to monitor the effect of PLEK2 on epithelial-mesenchymal transition (EMT) signalling pathways. PLEK2 expression was significantly upregulated in gastric cancer as compared with nontumour samples. Kaplan-Meier plotter analysis revealed that gastric cancer patients with higher PLEK2 levels had substantially poorer overall survival compared with gastric cancer patients with lower PLEK2 levels. The upregulation or downregulation of PLEK2 in gastric cancer cell lines effectively enhanced or inhibited cell proliferation and proinvasive behaviour, respectively. Additionally, we also found that PLEK2 enhanced EMT through downregulating E-cadherin expression and upregulating Vimentin expression. Our findings demonstrated that PLEK2 plays a potential role in gastric cancer and may be a novel therapeutic target for gastric cancer.http://dx.doi.org/10.1155/2021/5527387
spellingShingle Jun Wang
Zhigang He
Bo Sun
Wenhai Huang
Jianbin Xiang
Zongyou Chen
Zhenyang Li
Xiaodong Gu
Pleckstrin-2 as a Prognostic Factor and Mediator of Gastric Cancer Progression
Gastroenterology Research and Practice
title Pleckstrin-2 as a Prognostic Factor and Mediator of Gastric Cancer Progression
title_full Pleckstrin-2 as a Prognostic Factor and Mediator of Gastric Cancer Progression
title_fullStr Pleckstrin-2 as a Prognostic Factor and Mediator of Gastric Cancer Progression
title_full_unstemmed Pleckstrin-2 as a Prognostic Factor and Mediator of Gastric Cancer Progression
title_short Pleckstrin-2 as a Prognostic Factor and Mediator of Gastric Cancer Progression
title_sort pleckstrin 2 as a prognostic factor and mediator of gastric cancer progression
url http://dx.doi.org/10.1155/2021/5527387
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