IL-17 Affects the Progression, Metastasis, and Recurrence of Laryngeal Cancer via the Inhibition of Apoptosis through Activation of the PI3KAKTFASFASL Pathways

Abstract EN

Background.

Cytokines play important roles in the development and prognosis of laryngeal cancer (LC).

Interleukin-17 (IL-17) from a distinct subset of CD4+ T cells may significantly induce cancer-elicited inflammation to prevent tumor immune surveillance.

Methods.

The expression levels of IL-17 were examined among 60 patients with LC.

Immunofluorescence colocalization experiments were performed to verify the localization of IL-17 and FAS/FASL in Hep-2 and Tu212 cells.

The role of IL-17 was determined using siRNA techniques in the LC cell line.

Results.

In the LC patients, cytokines were dysregulated in LC tissues compared with normal tissues.

It was found that IL-17 was overexpressed in a cohort of 60 LC tumors paired with nontumor tissues.

Moreover, high IL-17 expression was significantly associated with the advanced T category, the late clinical stage, differentiation, lymph node metastasis, and recurrence.

In addition, the time course expression of FAS and FASL was observed after stimulation and treatment with the IL-17 stimulator.

Finally, in vitro experiments demonstrated that IL-17 functioned as an oncogene by inhibiting the apoptosis of LC cells via the PI3K/AKT/FAS/FASL pathways.

Conclusions.

In summary, these findings demonstrated for the first time the role of IL-17 as a tumor promoter and a prometastatic factor in LC and indicated that IL-17 may have an oncogenic role and serve as a potential prognostic biomarker and therapeutic target in LC.