Interleukin‑17 activates JAK2/STAT3, PI3K/Akt and nuclear factor‑κB signaling pathway to promote the tumorigenesis of cervical cancer
Yanfei Bai, Haitao Li, Rui Lv
Abstract
Interleukin (IL)‑17 has been regarded as a significant factor in inflammation. In addition, IL‑17 is known to be involved in the progression of cancers; however, the function of IL‑17 in cervical cancer remains unclear. In the present study, cell viability was detected by Cell Counting Kit‑8 assay. Quantitative PCR and western blotting were performed to detect gene and protein expression levels, respectively, in cancer cells or tissues. Ki‑67 staining was used to evaluate cell proliferation. Wound‑healing assay was used to detect cell migration. Moreover, Transwell assay was performed to investigate the invasion of cervical cancer cells. The results revealed that IL‑17 significantly promoted the proliferation of cervical cancer cells. Additionally, IL‑17 notably enhanced the migration and invasion of cervical cancer cells <em>in vitro</em>. IL‑17 promoted the progression of cervical cancer via the activation of JAK2/STAT3 and PI3K/Akt/NF‑κB signaling. In conclusion, IL‑17 was a key regulator during the progression of cervical cancer through the JAK2/STAT3 and PI3K/Akt/nuclear factor‑κB signaling pathway, which may serve as a novel target for the treatment of cervical cancer.