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 (MPD) and an unfavorable prognosis. Furthermore, the qPCR analysis revealed that human LC tissues overexpress signal transducers and activators of transcription 3 (STAT3), and the relevance analysis found this STAT3 overexpression had a significant correlation with IL-23R expression. Besides, we isolated and cultured IL-23R+ human tumor cells from the post-operation tumor sample of three LC patients, and found that rhIL-23 could phosphorylate STAT3 (pSTAT3, residue Y705), which resulted in cancer cell proliferation and cisplatin resistance. These results indicate that IL-23R was a Hallmark of cancer immunoediting process, and targeting IL-23 should be considered as a therapeutic option for laryngeal function preservation and survival improvement.
journal_name
Carcinogenesisjournal_title
Carcinogenesisauthors
Tao Y,Shen H,Liu Y,Li G,Huang Z,Liu Ydoi
10.1093/carcin/bgaa058subject
Has Abstractpub_date
2020-06-12 00:00:00eissn
0143-3334issn
1460-2180pii
5856155pub_type
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