Oral squamous cell carcinomas (OSCC) constitute over 95% of all head and neck
malignancies. As a key component of the tumor microenvironment (TME), chronic
inflammation contributes towards the development, progression, and regional
metastasis of OSCC. Tumor associated macrophages (TAMs) associated with OSSC promote
tumorigenesis through the production of
cytokines and pro-inflammatory factors that are critical role in the various steps of malignant transformation, including
tumor growth, survival, invasion, angiogenesis, and
metastasis. The
mitogen-activated protein kinases (MAPKs) can regulate
inflammation along with a wide range of cellular processes including cell metabolism, proliferation, motility, apoptosis, survival, differentiation and play a crucial role in cell growth and survival in physiological and
pathological processes including innate and adaptive immune responses. Dual specificity
MAPK phosphatases (MKPs) deactivates MAPKs. MKPs are considered as an important feedback control mechanism that limits MAPK signaling and subsequent target gene expression. This review outlines the role of MKP-1, the founding member of the MKP family, in OSCC and the TME. Herein, we summarize recent progress in understanding the regulation of
p38 MAPK/MKP-1 signaling pathways via TAM-related immune responses in OSCC development, progression and treatment outcomes.