ArticleMedical oncology (Northwood, London, England)2015
Endothelial cell protein C receptor promotes MGC803 gastric cancer cells proliferation and migration by activating ERK1/2.
Article in Medical oncology (Northwood, London, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- Gastric Cancer: Pathobiology and Therapeutics.MedComm · 2026Review
- Article
- Protease-Activated Receptor F2R Is a Potential Target for New Diagnostic/Prognostic and Treatment Applications for Patients with Ovarian Cancer.International journal of molecular sciences · 2025Article
- Mechanism of dexmedetomidine in inhibiting proliferation, migration, and invasion of esophageal squamous cell carcinoma cell through coagulation factor II receptor.Discover oncology · 2025Article
- New insights into vitamin K biology with relevance to cancer.Trends in molecular medicine · 2022Review
- Role of Extracellular High-Mobility Group Box-1 as a Therapeutic Target of Gastric Cancer.International journal of molecular sciences · 2022Article
- Tumor-associated macrophages (TAMs) depend on MMP1 for their cancer-promoting role.Cell death discovery · 2021Article
- Coagulation factor 2 thrombin receptor promotes malignancy in glioma under SOX2 regulation.Aging · 2020Article
- Review
- EPCR promotes MGC803 human gastric cancer cell tumor angiogenesisOncology letters · 2018Article
- Review
- Endothelial protein C receptor is overexpressed in colorectal cancer as a result of amplification and hypomethylation of chromosome 20q.The journal of pathology. Clinical research · 2017Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The endothelial cell protein C receptor (EPCR) has been reported to be involved in the development of several human cancers. However, the role of EPCR in gastric cancer progression has not been clarified. In this study, we show for the first time that EPCR is related to gastric cancer. Our results indicate that EPCR is highly expressed in clinical gastric cancer tissue. Knockdown of EPCR by small interference RNA suppressed the proliferation and migration of MGC803 gastric cancer cells dominantly. Blocking antibodies to protease-activated receptor-1(PAR1) also suppressed the proliferation and migration of MGC803 cells. Knockdown EPCR and blocking PAR1 inhibit activation of extracellular signaling-regulated kinases 1 and 2 (ERK1/2). Taken together, these results indicate that EPCR contributes to the proliferation and migration of MGC803 gastric cancer cells by activating ERK1/2, and this effect of EPCR may be dependent on PAR1. Therefore, EPCR may be act as a novel therapeutic target for inhibiting cell growth in gastric cancer.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.