IL-23R in laryngeal cancer: a cancer immunoediting process that facilitates tumor cell proliferation and results in cisplatin resistance.

Carcinogenesis
Ye TaoYehai Liu

Abstract

Oncogenic pathogens can disturb tissue homeostasis and initiate immune responses for oncogenicity clearance and homeostasis restoration, while failed clearance and chronic inflammation may result in tumorigenesis. The primary tumor development will undergo a cancer immunoediting process, including three phases, termed elimination, equilibrium and escape. Importantly, immune-edited tumor cells can not only reduce immunogenic molecular expression but also manipulate cytokines within the tumor environment (TME) for immune evasion and tumor proliferation. Many studies have revealed that IL-23R performed an essential role in mucous inflammation and tumorigenesis, and the role of IL-23R, either in tumor-infiltrating lymphocytes (TILs) or within immune-edited tumor cells, remained largely unknown in laryngeal cancer (LC). Here, we separately analyzed the IL-23R expression in LC TILs and tumor cells and found that high IL-23R expression in tumor cells was associated with moderate and poor tumor differentiation and an unfavorable prognosis. Furthermore, the real-time quantitative polymerase chain reaction analysis revealed that human LC tissues overexpress signal transducers and activators of transcription 3 (STAT3), and the relevance a...Continue Reading

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