Chemokine receptor CXCR7 expression, function and clinical implications in head and neck squamous cell carcinoma

Lee, M.-W.; Kim, N.; Kim, Seokhyeon; Joo, Mina; Ryu, Hyewon; Lee, H.J.

doi:10.1093/annonc/mdy304.037

Cited by 1 publication

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“…Cytokines, chemokines, and their receptors are important players of TME and are known for initiation, promotion, progression, metastasis, and development of aggressiveness [ 207 ]. For example, upregulation of CXCR7 increased cell migration and invasion through the Smad2/Akt signaling pathway, promoted lymph node metastasis [ 208 ], and is associated with the aggressive phenotype of HNSCC [ 187 ]. Further studies showed that CCR7 in HNSCC is upregulated by NF-kB and AP1 and contributes to metastatic phenotype [ 209 ].…”

Section: Chemokines and Cytokines Promote Aggressive Hnscc Phenotypementioning

confidence: 99%

Chemokine-Cytokine Networks in the Head and Neck Tumor Microenvironment

Nisar

Yousuf

Masoodi³

et al. 2021

IJMS

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Head and neck squamous cell carcinomas (HNSCCs) are aggressive diseases with a dismal patient prognosis. Despite significant advances in treatment modalities, the five-year survival rate in patients with HNSCC has improved marginally and therefore warrants a comprehensive understanding of the HNSCC biology. Alterations in the cellular and non-cellular components of the HNSCC tumor micro-environment (TME) play a critical role in regulating many hallmarks of cancer development including evasion of apoptosis, activation of invasion, metastasis, angiogenesis, response to therapy, immune escape mechanisms, deregulation of energetics, and therefore the development of an overall aggressive HNSCC phenotype. Cytokines and chemokines are small secretory proteins produced by neoplastic or stromal cells, controlling complex and dynamic cell–cell interactions in the TME to regulate many cancer hallmarks. This review summarizes the current understanding of the complex cytokine/chemokine networks in the HNSCC TME, their role in activating diverse signaling pathways and promoting tumor progression, metastasis, and therapeutic resistance development.

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