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Up and away with cervical cancer: IL-29 is a promising cytokine for immunotherapy of cervical cancer due to its powerful upregulation of p18, p27, and TRAILR1

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Abstract

Cervical cancer is one of the most common types of female cancers worldwide. IL-29 is an interesting cytokine in the IFNλ family. Its role in the pathogenesis of neoplasia is complicated and has been studied in other cancers, such as lung cancer, gastric cancer, and colorectal cancer. IL-29 has been previously reported to promote the growth of pancreatic cancer. However, the direct role of IL-29 in cervical cancer has not been studied yet. This study was performed to investigate the direct effect on cervical cancer cell growth. Clonogenic survival assay, cell proliferation, and caspase-3 activity kits were used to evaluate the effects of IL-29 on cell survival, proliferation, and apoptosis of a well-studied cervical cancer cell line, SiHa. We further investigated the potential molecular mechanisms by using RT-PCR and IHC. We found that the percentage of colonies of SiHa cells was decreased in the presence of IL-29. This was consistent with a decreased OD value of cancer cells. Furthermore, the relative caspase-3 activity in cancer cells increased in the presence of IL-29. The anti-proliferative effect of IL-29 on cancer cells correlated with increased expression of the anti-proliferative molecules p18 and p27. The pro-apoptotic effect of IL-29 on cancer cells correlated with increased expression of the pro-apoptotic molecule TRAILR1. IL-29 inhibits cervical cancer cell growth by inhibiting cell proliferation and promoting cell apoptosis. Thus, IL-29 might be a promising cytokine for immunotherapy of cervical cancer.

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Funding

This work was supported by a Grant IOER 112–3749 from Des Moines University for Yujiang Fang.

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Correspondence to Lijun Dong or Yujiang Fang.

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Ha, J.L., Kaser, E., Guan, T. et al. Up and away with cervical cancer: IL-29 is a promising cytokine for immunotherapy of cervical cancer due to its powerful upregulation of p18, p27, and TRAILR1. Med Oncol 41, 65 (2024). https://doi.org/10.1007/s12032-023-02276-3

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