Sdcbp, also known as syndecan binding protein or syntenin1, is an adapter protein with two tandem PDZ domains, essential for cell adhesion, migration, and signal transduction [2,5]. It is involved in multiple cellular processes and associated with various pathways such as the EGFR-PI3K-Akt signaling pathway [5]. Its dysregulation has significant implications in multiple diseases, making it an important gene for biological and medical research.

In pancreatic ductal adenocarcinoma (PDAC), Sdcbp promotes tumor progression by preventing YAP1 from β-TrCP-mediated proteasomal degradation. In preclinical KPC mouse cohorts, zinc pyrithione (ZnPT) suppresses PDAC tumor progression by suppressing Sdcbp [1]. In colorectal cancer, high Sdcbp expression is related to non-response to immunotherapy and poor disease-free survival. Inhibiting Sdcbp with shRNA or ZnPT hindered tumor proliferation and metastasis and enhanced anti-PD1 treatment efficacy in mouse models [3]. In head and neck squamous cell carcinoma, Sdcbp depletion sensitized cells to cisplatin, reduced cancer stem cell markers, and in mice, Sdcbp-depleted cells formed tumors with decreased mitosis and metastasis [4].

In conclusion, Sdcbp plays a crucial role in promoting tumor progression in multiple cancers, including PDAC, colorectal cancer, and head and neck squamous cell carcinoma. Studies using mouse models, such as KPC mice in PDAC research, have been instrumental in revealing Sdcbp's functions in disease processes, highlighting its potential as a therapeutic target for cancer treatment.