DKK1 in Cancer: A Bench-to-Bedside Review of Molecular Mechanisms and Clinical Applications
Dickkopf-1 (DKK1) is a secreted glycoprotein that traditionally acts as an antagonist of canonical Wnt/β-catenin signaling. Although it functions as a tumor suppressor in some specific biological background and disease stages, growing evidence links DKK1 to tumor progression, immune evasion, and therapy resistance in a variety of multiple malignancies. This review provides a comprehensive bench-to-bedside overview of DKK1 in cancer. We first delineate how DKK1 regulates both Wnt-dependent and Wnt-independent pathways. From a clinical perspective, we evaluate the application potential of DKK1 as a diagnostic and prognostic biomarker. We further discuss the progress of DKK1-targeted interventions, ranging from monoclonal antibodies in clinical trials to next-generation therapeutic modalities. Finally, we discuss the challenges in clinical translation and suggest future directions for DKK1-based precision medicine. In summary, by integrating preclinical insights with current clinical data, this review provides a strategic roadmap for advancing DKK1-targeted therapies in cancer.
Authors
- Bao‐Ting Zhang (ORCID: https://orcid.org/0000-0003-1421-0212)
- Y S Zhang
- Meiheng Sun (ORCID: https://orcid.org/0000-0003-2197-0439)
- Ge Zhang (ORCID: https://orcid.org/0000-0002-7807-7695)
- Wei Kang
- Ziqi Chen
- Yuzhe Wang
- Qianjun Chen
- Jianhui Tian
- Yuanyuan Yu
- Aiping Lu
Institutions
- Guangzhou University of Chinese Medicine (CN)
- Hong Kong Baptist University (HK)
- Chinese University of Hong Kong (HK)
- Shanghai University of Traditional Chinese Medicine (CN)
- Guangdong Provincial Hospital of Traditional Chinese Medicine (CN)
- Prince of Wales Hospital (CN)
- Shanghai Traditional Chinese Medicine Hospital (CN)
Publication Details
- Journal
- Cancers
- Published
- 2026-04-25
- DOI
- https://doi.org/10.3390/cancers18091375
- Primary Topic
- Wnt/β-catenin signaling in development and cancer
- Type
- article
- Field-Weighted Citation Impact
- 0.00