Research Progress on the Relationship Between WSTF and Cancer
DOI:
https://doi.org/10.71204/mny7mr80Keywords:
WSTF, Malignant Tumors, Transcriptional Regulation, PI3K/Akt PathwayAbstract
The Williams syndrome transcription factor (WSTF, alternatively termed BAZ1B) represents a versatile nuclear protein that exerts pleiotropic effects on neurodevelopmental processes, chromatin remodeling, DNA damage repair, as well as transcriptional regulation. Accumulating evidence demonstrates that WSTF is a crucial molecular determinant in the pathogenesis and progression of multiple cancers, positioning it as a viable therapeutic target. This review systematically synthesizes the molecular mechanisms by which WSTF drives oncogenesis across malignancies, focusing on its interplay with regulatory factors and signaling pathways. In breast cancer, WSTF participates in estrogen receptor (ER) signaling and contributes to endocrine therapy resistance by modulating ER-dependent gene expression to promote proliferation and invasion. WSTF also interacts with the vitamin D analog EB1089, suppressing tumor progression through altered promoter binding. In gastric cancer, aberrant WSTF expression disrupts cell adhesion, increasing cancer cell dependency on WSTF. Hyperphosphorylation of WSTF in diffuse gastric cancer further implicates it in tumorigenesis. In cervical, glioblastoma, and lung cancers, WSTF activates the PI3K-Akt signaling cascade, enhancing tumor cell proliferation, migration, and invasion. These findings underscore WSTF’s oncogenic role and therapeutic potential. Further investigation into WSTF’s functions and regulatory mechanisms will deepen our understanding of tumorigenesis and inform novel therapies targeting this chromatin regulator.
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