OX-40 signaling promotes tumorigenesis in CTCL by regulating ERK activation
Using the CTCL spontaneous metastasis model in chick embryos, we demonstrated that OX-40 regulates the TME to promote M2 increase, lymphangiogenesis, CAM intravasation, and metastasis. Therefore, the <i>in vivo</i> chick embryo metastasis model may serve as a valuable preclinical tool for identifying novel anti-tumor targets in CTCL. The OX-40 axis was identified as a key driver of CTCL progression, promoting tumor growth and metastasis through ERK activation while validating the chick embryo model as a preclinical tool for therapeutic testing.
Authors
- Christina Piperi (ORCID: https://orcid.org/0000-0002-2701-0618)
- Fani Karagianni (ORCID: https://orcid.org/0000-0001-9514-2199)
- Berta Casar (ORCID: https://orcid.org/0000-0002-3058-5631)
- Evangelia Papadavid (ORCID: https://orcid.org/0000-0002-8634-102X)
- Eleni‐Kyriaki Vetsika (ORCID: https://orcid.org/0000-0002-3994-1583)
- Sara Valero-Dıáz (ORCID: https://orcid.org/0009-0005-6609-8447)
- Saire Edith Córdova-Hernández
- Christos Daniil
Institutions
- National and Kapodistrian University of Athens (GR)
- Instituto de Biomedicina y Biotecnología de Cantabria (ES)
- University General Hospital Attikon (GR)
- Centro de Investigación Biomédica en Red de Cáncer (ES)
Publication Details
- Journal
- Frontiers in Immunology
- Published
- 2025-10-27
- DOI
- https://doi.org/10.3389/fimmu.2025.1677140
- Primary Topic
- Cutaneous lymphoproliferative disorders research
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- Centro de Investigación Biomédica en Red de Cáncer
- Instituto de Salud Carlos III