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Updated: Oct 17, 2025
Intramucosal Inoculation of Squamous Cell Carcinoma Cells in Mice for Tumor Immune Profiling and Treatment Response Assessment
Published on: April 22, 2019
Targeting-YAP/TAZ therapies for head and neck cancer, directly or indirectly?
1State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases & Chinese Academy of Medical Sciences Research Unit of Oral Carcinogenesis and Management & West China Hospital of Stomatology, Sichuan University, Chengdu 610041, China.
Abstract:
YAP/TAZ are wild over-activated in head and neck squamous cell carcinoma (HNSCC) with high potential as a direct therapy target for HNSCC treatments. However, the efforts on the directly targeting-YAP/TAZ therapies over the past decade, have very limited impacts, mainly caused by: 1. There is still none effective and specific YAP/TAZ inhibitor with clinical potential; 2. YAP/TAZ might not be directly targeted, because of their multiple important biological functions, such as: regulation of cell proliferation and survival, stem cell maintain, regulation of organ development, organ size control, and tissue regeneration. Interestingly, the over-activation of YAP/TAZ in HNSCC mainly be regulated by upstream abnormal molecular or biological events, instead of genes alteration of YAP/TAZ. Therefore, exploring the alternative molecular events regulating YAP/TAZ activation and molecular mechanism in HNSCC might help to uncover novel indirect targets of YAP/TAZ therapies for HNSCC prevention and treatment.
Insights
Overactive YAP/TAZ proteins in head and neck cancer are a treatment challenge. Targeting upstream regulators offers a promising new strategy for HNSCC therapies.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Yeast And Protein Associated (YAP) and Tafazzin (TAZ) are frequently overactive in head and neck squamous cell carcinoma (HNSCC).
- Directly targeting YAP/TAZ for HNSCC treatment has shown limited success due to a lack of specific inhibitors and their crucial physiological roles.
- YAP/TAZ overactivation in HNSCC often stems from upstream events rather than direct gene alterations.
Purpose of the Study:
- To investigate alternative molecular mechanisms that regulate YAP/TAZ activation in HNSCC.
- To identify novel indirect therapeutic targets for HNSCC prevention and treatment by understanding upstream regulators of YAP/TAZ.
Main Methods:
- The study likely involved analyzing molecular pathways and biological events upstream of YAP/TAZ in HNSCC models.
- Investigating the correlation between these upstream events and YAP/TAZ activity.
Main Results:
- YAP/TAZ overactivation in HNSCC is primarily driven by upstream molecular alterations.
- These upstream events represent potential indirect targets for therapeutic intervention.
Conclusions:
- Directly targeting YAP/TAZ in HNSCC is challenging.
- Focusing on upstream regulators of YAP/TAZ offers a more viable strategy for developing novel HNSCC therapies.
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