The role of formin-like protein 1 in pancreatic cancer and its specific effects on immunity
ObjectiveTo investigate the functions and immunological implication of formin-like protein 1 in pancreatic cancer.MethodsA multitude of public datasets and an in-house cohort were used to assess the clinical relevance and the immunological relevance of formin-like protein 1 in pancreatic cancer. Subsequently, in vitro assays were conducted to evaluate the biological roles of formin-like protein 1 in pancreatic cancer and its effects on immunity.ResultsThe expression of formin-like protein 1 was elevated in pancreatic cancer tissues and linked to a poor prognosis in pancreatic cancer. In vitro assays showed that elevated expression of formin-like protein 1 promoted pancreatic cancer progression. Moreover, formin-like protein 1 was linked to an inflamed tumor microenvironment and mediated epithelial-mesenchymal transition and programmed cell death 1 ligand 1 expression in pancreatic cancer.ConclusionsFormin-like protein 1 is a biomarker of an inflamed tumor microenvironment and positively modulates epithelial-mesenchymal transition and programmed cell death 1 ligand 1 expression in pancreatic cancer, which could be utilized as a novel target for antitumor immunity for more in-depth studies.
Authors
- Shoupeng Shao
- Xuejing Yang (ORCID: https://orcid.org/0000-0002-4620-1284)
- Jie Mei (ORCID: https://orcid.org/0000-0001-9521-4287)
- Liang Chen (ORCID: https://orcid.org/0000-0002-7985-4273)
- Jian Liu (ORCID: https://orcid.org/0000-0002-1447-0973)
- Junli Ding
Institutions
- Nantong University (CN)
- Affiliated Hospital of Nantong University (CN)
- Yancheng First People's Hospital (CN)
- Yancheng Third People's Hospital (CN)
- Wuxi People's Hospital (CN)
- Nanjing Medical University (CN)
Publication Details
- Journal
- Journal of International Medical Research
- Published
- 2025-08-01
- DOI
- https://doi.org/10.1177/03000605251365844
- Primary Topic
- Pancreatic and Hepatic Oncology Research
- Type
- article
- Field-Weighted Citation Impact
- 0.00