Open Access<p>Role of Focal Adhesion Kinase in Head and Neck Squamous Cell Carcinoma and Its Therapeutic Prospect</p>
Author(s) -
Yuxi Zhang,
Xinchen Sun
Publication year - 2020
Publication title -
oncotargets and therapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.054
H-Index - 60
ISSN - 1178-6930
DOI - 10.2147/ott.s270342
Subject(s) - head and neck squamous cell carcinoma , cancer research , medicine , focal adhesion , metastasis , carcinogenesis , tumor progression , cell , radiation therapy , oncology , pathology , cancer , head and neck cancer , biology , genetics
Head and neck cancers are one of the most prevalent cancers globally. Among them, head and neck squamous cell carcinoma (HNSCC) accounts for approximately 90% of head and neck cancers, which occurs in the oral cavity, oral pharynx, hypopharynx and larynx. The 5-year survival rate of HNSCC patients is only 63%, mainly because about 80-90% of patients with advanced HNSCC tend to suffer from local recurrence or even distant metastasis. Despite the more in-depth understanding of the molecular mechanisms underlying the occurrence and progression of HNSCC in recent years, effective targeted therapies are unavailable for HNSCC, which emphasize the urgent demand for studies in this area. Focal adhesion kinase (FAK) is an intracellular non-receptor tyrosine kinase that contributes to oncogenesis and tumor progression by its significant function in cell survival, proliferation, adhesion, invasion and migration. In addition, FAK exerts an effect on the tumor microenvironment, epithelial-mesenchymal transition, radiation (chemotherapy) resistance, tumor stem cells and regulation of inflammatory factors. Moreover, the overexpression and activation of FAK are detected in multiple types of tumors, including HNSCC. FAK inhibition can induce cell cycle arrest and apoptosis, significantly decrease cell growth, invasion and migration in HNSCC cell lines. In this article, we mainly review the research progress of FAK in the occurrence, development and metastasis of HNSCC, and put forward the prospects for the therapeutic targets of HNSCC.