ArticleGastroenterology research and practice2021
Pleckstrin-2 as a Prognostic Factor and Mediator of Gastric Cancer Progression.
Article in Gastroenterology research and practice, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Pleckstrin-2 Mediates the Activation of AKT in Prostate Cancer and Is Repressed by Androgen Receptor.The American journal of pathology · 2024Article
- PLEK2: a potential biomarker for metastasis and prognostic evaluation in uveal melanoma.Frontiers in medicine · 2024Article
- LWJ-M30, a conjugate of DM1 and B6, for the targeted therapy of colorectal cancer with improved therapeutic effects.RSC advances · 2023Article
- Targeting pleckstrin-2/Akt signaling reduces proliferation in myeloproliferative neoplasm models.The Journal of clinical investigation · 2023Article
- PLEK2 promotes cancer stemness and tumorigenesis of head and neck squamous cell carcinoma via the c-Myc-mediated positive feedback loop.Cancer communications (London, England) · 2022Article
- Identification of hub genes of Parkinson's disease through bioinformatics analysis.Frontiers in neuroscience · 2022Article
- Pleckstrin 2 is a potential drug target for colorectal carcinoma with activation of APC/β‑catenin.Molecular medicine reports · 2021Article
- Emerging Roles of Pleckstrin-2 Beyond Cell Spreading.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
Identifiers
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Registered trials
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