SHIP2–PLK1 crosstalk promotes sensitivity to dual inhibition in esophageal squamous cell carcinoma
Our data support the use of specific SHIP2 inhibitors, in combination with PLK1 inhibitors, as a promising strategy for stalling eSCC growth, amplifying treatment response, and circumventing resistance. This study unravels the intricate interplay of SHIP2 within the PI3K/AKT pathway and cell cycle in eSCC, paving the way for targeted interventions with the potential to transform the therapeutic landscape of this challenging malignancy.
Authors
- Sheleya Pirard (ORCID: https://orcid.org/0000-0001-9151-2754)
- Giacomo Bregni (ORCID: https://orcid.org/0000-0002-4051-0449)
- Kunié Ando (ORCID: https://orcid.org/0000-0003-3822-175X)
- Christophé Erneux (ORCID: https://orcid.org/0000-0002-0773-8206)
- Xavier Bisteau (ORCID: https://orcid.org/0000-0002-8896-5098)
- Alizée Vercauteren Drubbel (ORCID: https://orcid.org/0000-0002-6365-3418)
- Fabiana Moresi (ORCID: https://orcid.org/0000-0002-1244-5571)
- Nadia Gillet
- B. Beck
- Ana Raquel Ramos
- Louison Descampe
- Quentin Verheye
- Cyril Bodart
Institutions
- University of Béjaïa (DZ)
- Institut Jules Bordet (BE)
- Directorate-General Joint Research Centre (BE)
Publication Details
- Journal
- Molecular Cancer
- Published
- 2025-11-04
- DOI
- https://doi.org/10.1186/s12943-025-02454-z
- Citations
- 1
- Primary Topic
- PI3K/AKT/mTOR signaling in cancer
- Type
- article
- Field-Weighted Citation Impact
- 0.81
Funders
- Fonds De La Recherche Scientifique - FNRS
- Masarykova Univerzita
- Walloon excellence in life sciences and biotechnology