Epithelial-Mesenchymal Transition Associated with Head and Neck Squamous Cell Carcinomas: A Review

Simple Summary Mesenchymal conversion occurring in malignant epithelial neoplasms is undesirable in tumors since it promotes more aggressive tumor behavior. This phenomenon is not exclusive to head and neck carcinomas, and it is likely to be found in most neoplasms, as carcinomas are frequently aggressive. Mesenchymal conversion depends on different molecular interactions, signaling pathways, and tumor microenvironments that are related to the activation of several growth factors and diverse matrix metalloproteinases that promote ideal environments for the progression of tumor cells that are primarily associated with metastasis. This manuscript aims to review the interactions of the main molecules related to EMT. Head and neck squamous cell carcinomas (HNSCCs) are aggressive, recurrent, and metastatic neoplasms with a high occurrence around the world and can lead to death when not treated appropriately. Several molecules and signaling pathways are involved in the malignant conversion process. Epithelial-mesenchymal transition (EMT) has been described in HNSCCs, a major type of aggressive carcinoma. EMT describes the development of epithelial cells into mesenchymal cells, which depends on several molecular interactions and signaling pathways that facilitate mesenchymal conversion. This is related to interactions with the microenvironment of the tumor, hypoxia, growth factors, matrix metalloproteinases, and the presence of viral infections. In this review, we focus on the main molecules related to EMT, their interactions with the tumor microenvironment, plasticity phenomena, epigenetic regulation, hypoxia, inflammation, their relationship with immune cells, and the inhibition of EMT in the context of HNSCCs.

Automated summary

Mesenchymal conversion occurring in malignant epithelial neoplasms promotes aggressive tumor behavior. Head and neck squamous cell carcinomas are aggressive, recurrent, and metastatic neoplasms involving various molecules and signaling pathways in the malignant conversion process. The review focuses on main molecules related to EMT, interactions with the tumor microenvironment, epigenetic regulation, hypoxia, inflammation, immune cell relationships, and EMT inhibition in the context of HNSCCs.