HGF/Met and the Head and Neck Cancer Microenvironment

Studies to date have revealed several major molecular alterations that contribute to head and neck squamous cell carcinoma (HNSCC) initiation, progression, metastatic spread and therapeutic failure. The epidermal growth factor receptor (EGFR) is the only FDA-approved therapeutic target yet responses to cetuximab have been limited. Activation and crosstalk of cellular receptors and consequent activation of different signaling pathways contributes to limited activity of blockade of a single pathway. The hepatocyte growth factor (HGF) receptor, Met has been implicated in HNSCC tumorigenesis and EGFR inhibitor resistance. HGF, the sole ligand of Met, is overexpressed in the tumor microenvironment. The role of HGF/Met signaling in proliferation, metastasis and angiogenesis has been investigated in HNSCC leading to clinical trials with various Met inhibitors and HGF antibodies. However, the role of the HGF/Met signaling axis in mediating the tumor microenvironment has been relatively understudied in HNSCC. In this review we will discuss the functional roles of Met and HGF in HNSCC with a focus on the tumor microenvironment and the immune system.

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