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
Affiliations: Department of Obstetrics and Gynecology, Lanzhou Second People's Hospital, Lanzhou, Gansu 730000, P.R. China, Department of Gynecology, Affiliated Hospital of Gansu Medical College, Lanzhou, Gansu 744000, P.R. China, Department of Gynecologic Oncology, Gansu Provincial Cancer Hospital, Lanzhou, Gansu 730030, P.R. China
- Published online on: September 13, 2021 https://doi.org/10.3892/etm.2021.10726
Copyright: © Bai
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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.