The dual role of interleukin-17 in the growth of human papillomavirus-negative cervical cancer cells

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Abstract

To explore the relationship between IL-17 mediated immune response and HPV-negative cervical cancer, we established the co-culture system of cervical cancer C-33A cells and PBMC, and treated with different concentrations of rhIL-17. PBMC were extracted from 10ml anticoagulant blood provided by healthy female volunteers and colleagues in our hospital, which were co-cultured with cervical cancer C-33A cells. After treatment with different concentrations of rhIL-17, the proliferation, apoptosis, invasion behavior and VEGF expression level of cancer cells in each group, were determined by CCK-8, flow cytometry, transwell invasion assay and ELISA, respectively. The proliferation rate of C-33A cells slightly increased with the ascending of IL-17 concentration, but no statistical significance was found among each group (P > 0.05). When at low concentration of IL-17, the cell apoptosis rate seems to slightly decline. With the increase of concentration, the decrease of apoptosis rate became more obvious (P < 0.05). However, differing from those shown above, we found that IL-17 slightly inhibited the cancer cell invasion at high concentration, while it was more obvious at low concentration (P < 0.05). Furthermore, we found that there was no significant correlation between IL-17 and VEGF (P > 0.05). In summary, there is a close correlation between IL-17 mediated immune response and HPV-negative cervical cancer. Also, we think that IL-17 may play a dual role in tumor progression and could be a possible significant influence on tumor proliferation, apoptosis, and metastasis, which provides a basic theoretical basis for the further study of immunotherapy measures for cervical cancer.

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Pan, Y., Luo, X., Ma, J., Feng, Z., Hu, Y., & Xue, J. (2022). The dual role of interleukin-17 in the growth of human papillomavirus-negative cervical cancer cells. European Journal of Inflammation, 20. https://doi.org/10.1177/1721727X221128089

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