Interleukin-17 activates JAK2/STAT3, PI3K/Akt and nuclear factor-κB signaling pathway to promote the tumorigenesis of cervical cancer

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 in vitro. 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.