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Published on: April 22, 2019
MERTK as a novel therapeutic target in head and neck cancer
Anne von Mässenhausen1,2,3, Christine Sanders1,2,3, Britta Thewes1,2,3
1Section of Prostate Cancer Research, University Hospital of Bonn, Bonn, Germany.
Abstract:
Although head and neck cancer (HNSCC) is the sixth most common tumor entity worldwide therapy options remain limited leading to 5-year survival rates of only 50 %. MERTK is a promising therapeutic target in several tumor entities, however, its role in HNSCC has not been described yet. The aim of our study was to investigate the biological significance of MERTK and to evaluate its potential as a novel therapeutic target in this dismal tumor entity. In two large HNSCC cohorts (n=537 and n=520) we found that MERTK is overexpressed in one third of patients. In-vitro, MERTK overexpression led to increased proliferation, migration and invasion whereas MERTK inhibition with the small molecule inhibitor UNC1062 or MERTK knockdown reduced cell motility via the small GTPase RhoA.Taken together, we are the first to show that MERTK is frequently overexpressed in HNSCC and plays an important role in tumor cell motility. It might therefore be a potential target for selected patients suffering from this dismal tumor entity.
Insights
Head and neck squamous cell carcinoma (HNSCC) shows limited treatment options. Our study reveals MERTK overexpression drives HNSCC cell motility, suggesting MERTK as a potential therapeutic target for improving patient outcomes.
Area of Science:
- Oncology
- Molecular Biology
Background:
- Head and neck squamous cell carcinoma (HNSCC) has poor survival rates.
- Therapeutic options for HNSCC are limited.
- The role of MERTK in HNSCC is currently unknown.
Purpose of the Study:
- Investigate the biological significance of MERTK in HNSCC.
- Evaluate MERTK as a potential therapeutic target for HNSCC.
Main Methods:
- Analysis of MERTK expression in two large HNSCC patient cohorts (n=537 and n=520).
- In vitro experiments assessing the effects of MERTK overexpression and inhibition (UNC1062, MERTK knockdown) on cancer cell behavior.
- Investigation of downstream signaling pathways, including the small GTPase RhoA.
Main Results:
- MERTK is overexpressed in approximately one-third of HNSCC patients.
- MERTK overexpression enhances cancer cell proliferation, migration, and invasion.
- Inhibition of MERTK reduces cancer cell motility, involving the RhoA pathway.
Conclusions:
- MERTK is frequently overexpressed in HNSCC.
- MERTK plays a significant role in HNSCC cell motility.
- MERTK inhibition represents a potential therapeutic strategy for a subset of HNSCC patients.
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