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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Bibliographic Details
Published in:Gastroenterology research and practice 2021, Vol.2021, p.1-14
Main Authors: Wang, Jun, He, Zhigang, Sun, Bo, Huang, Wenhai, Xiang, Jianbin, Chen, Zongyou, Li, Zhenyang, Gu, Xiaodong
Format: Article
Language:English
Subjects:
Antibodies
Cancer
Cancer patients
Cloning
Development and progression
Experiments
Gastric cancer
Gene expression
Health aspects
Metastasis
Oncology, Experimental
Prognosis
Proteins
Stomach cancer
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Summary: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.
ISSN:1687-6121
1687-630X
DOI:10.1155/2021/5527387