ArticleExperimental physiology2023
Podoplanin promotes the carcinogenicity of gastric cancer by activating ezrin and mediating the crosstalk between tumour cells and cancer-associated fibroblasts.
Article in Experimental physiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- Stromal Cell Subsets Show Model-Dependent Changes in Experimental Colitis and Affect Epithelial Tissue Repair and Immune Cell Activation.Inflammatory bowel diseases · 2025Article
- PDPN+ cancer-associated fibroblasts enhance gastric cancer angiogenesis via AKT/NF-κB activation and the CCL2-ACKR1 axis.MedComm · 2025Article
- Knockdown of PDPN in astrocytes reduces hippocampal inflammation in T2DM mice.Frontiers in immunology · 2025Article
- The regulation of cancer-associated thrombosis by podoplanin.Thrombosis update · 2024Article
- Article
- Podoplanin promotes the carcinogenicity of gastric cancer by activating ezrin and mediating the crosstalk between tumour cells and cancer-associated fibroblasts.Experimental physiology · 2023Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
NEW
findingsWhat is the central question of this study? To reveal the role and biological mechanism of PDPN in the progression of gastric cancer. What is the main finding and its importance? This study focused on a prognostic predictor, PDPN, which acted as a promoter in the progression of gastric cancer through the activation of Ezrin expression and CAFs. This finding may expand a new route for the gene-targeted therapy in gastric cancer. ABSTRACT: Gastric cancer (GC) is a frequent malignant disease and the main cause of cancer-related death in the world. Podoplanin (PDPN) has been proved to be involved in the progression of various cancers. However, the role and biological mechanism of PDPN in GC are still vague. In our study, we detected the expression of PDPN in GC tissues and cell lines using RT-qPCR, western blot and datasets. The overall survival of GC patients was analysed with a Kaplan-Meier plot. The effects of PDPN overexpression and silencing on GC cell progression were assessed by Cell Counting Kit-8, flow cytometry and a wound healing assay. Besides, the modulation of PDPN on ezrin activation was investigated. We further explored the role of PDPN in the crosstalk between GC cells and cancer associated fibroblasts (CAFs). Results showed that PDPN was upregulated in GC tissues and cell lines. High expression of PDPN was correlated with poor prognosis of GC patients. PDPN positively regulated the viability, migration and invasion, but inhibited apoptosis, of GC cells by mediating the activation of ezrin. Meanwhile, the change in PDPN in GC cells activated CAFs and promoted the production of cytokines secreted by CAFs, which induced the progression of GC cells. These findings may provide a novel target for GC therapy.
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