ArticleExperimental and therapeutic medicine2015
EBP50 inhibits pancreatic cancer cell growth and invasion by targeting the β-catenin/E-cadherin pathway.
Article in Experimental and therapeutic medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Functional Roles and Mechanistic Insights of YEATS Domain Proteins in Digestive System Tumors.Digestive diseases and sciences · 2025Review
- Unveiling the role of GAS41 in cancer progression.Cancer cell international · 2023Review
- Identification of Moesin (MSN) as a Potential Therapeutic Target for Colorectal Cancer via the β-Catenin-RUNX2 Axis.International journal of molecular sciences · 2023Article
- Calpain2 Upregulation Regulates EMT-Mediated Pancreatic Cancer MetastasisFrontiers in medicine · 2022Article
- Histone methylation in pancreatic cancer and its clinical implications.World journal of gastroenterology · 2021Review
- PRMT1 promotes pancreatic cancer growth and predicts poor prognosis.Cellular oncology (Dordrecht, Netherlands) · 2020Article
- NHERF1 Between Promises and Hopes: Overview on Cancer and Prospective Openings.Translational oncology · 2018Review
- Sirtuin 7 promotes colorectal carcinoma proliferation and invasion through the inhibition of E-cadherin.Experimental and therapeutic medicine · 2018Article
- YEATS4 promotes the tumorigenesis of pancreatic cancer by activating beta-catenin/TCF signaling.Oncotarget · 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
Ezrin-radixin-moesin (ERM)-binding phosphoprotein 50 (EBP50) has previously been demonstrated to be associated with the malignant transformation of numerous types of human cancer. The aim of the present study was to investigate the effect of EBP50 overexpression on pancreatic cancer and the underlying mechanism. Reverse transcription-quantitative polymerase chain reaction was used to detect the expression of EBP50 in human pancreatic cancer tissue specimens. Furthermore, pBK-CMV-HA-EBP50 and the pBK-CMV-HA vectors were transfected into pancreatic cancer cells and the effect of EBP50 upregulation on the proliferation and invasion of the cells was investigated. In addition, the effect of EBP50 overexpression on β-catenin and E-cadherin expression was evaluated. The results revealed that overexpression of EBP50 suppressed cell growth and invasion in two human pancreatic cancer cell lines. Overexpression of EBP50 also suppressed β-catenin expression and increased E-cadherin expression. Thus, the present study demonstrated that EBP50 inhibits pancreatic cancer cell growth and invasion through targeting the β-catenin/E-cadherin pathway. The results suggest that EBP50 may function as a potential tumor suppressor and thus may serve as a potential therapeutic target.
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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.