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<p>This study investigates the role of Th17 cells and IL-17 signaling in mediating therapeutic resistance and early recurrence in cervical carcinoma. Th17 cells were generated in vitro, and cervical carcinoma cells were subsequently exposed to cisplatin in the presence of Th17-conditioned media or recombinant IL-17. To elucidate the underlying molecular mechanisms, synthetic siRNAs targeting Akt1 (si-Akt1) and Akt2 (si-Akt2) were employed. Gene expression levels were quantified using ABIVII7 qRT-PCR, and phosphorylation of AKT at Thr308 and Ser473 was assessed. Cervical carcinoma cell lines (HeLa and SW756) were cultured and subjected to siRNA-mediated knockdown of AKT1 and AKT2. Cytotoxicity assays were conducted to evaluate cell viability under various treatment conditions. Cells were stimulated with either standard medium or conditioned medium from in vitro–differentiated Th17 cells. Th17 cell–induced resistance to cisplatin and radiation co-treatment was found to be mediated via the AKT signaling pathway. Moreover, Th17 cells promoted chemoradiotherapy tolerance in cervical cancer cells, with a potential contribution from IL-17 signaling. Although chemoradiotherapy significantly decreased cell viability across all cell lines, preconditioning with recombinant IL-17 notably mitigated this effect, resulting in increased cellular survival. These findings suggest a critical role for Th17 cells in modulating the therapeutic response and recurrence risk in cervical carcinoma through AKT pathway activation.</p>

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Chemoradiotherapy-induced Th17/IL-17 signaling correlates with therapeutic tolerance and early recurrence in cervical carcinoma

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月6日

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  • Fanglei Cao,
  • Na Li

摘要

This study investigates the role of Th17 cells and IL-17 signaling in mediating therapeutic resistance and early recurrence in cervical carcinoma. Th17 cells were generated in vitro, and cervical carcinoma cells were subsequently exposed to cisplatin in the presence of Th17-conditioned media or recombinant IL-17. To elucidate the underlying molecular mechanisms, synthetic siRNAs targeting Akt1 (si-Akt1) and Akt2 (si-Akt2) were employed. Gene expression levels were quantified using ABIVII7 qRT-PCR, and phosphorylation of AKT at Thr308 and Ser473 was assessed. Cervical carcinoma cell lines (HeLa and SW756) were cultured and subjected to siRNA-mediated knockdown of AKT1 and AKT2. Cytotoxicity assays were conducted to evaluate cell viability under various treatment conditions. Cells were stimulated with either standard medium or conditioned medium from in vitro–differentiated Th17 cells. Th17 cell–induced resistance to cisplatin and radiation co-treatment was found to be mediated via the AKT signaling pathway. Moreover, Th17 cells promoted chemoradiotherapy tolerance in cervical cancer cells, with a potential contribution from IL-17 signaling. Although chemoradiotherapy significantly decreased cell viability across all cell lines, preconditioning with recombinant IL-17 notably mitigated this effect, resulting in increased cellular survival. These findings suggest a critical role for Th17 cells in modulating the therapeutic response and recurrence risk in cervical carcinoma through AKT pathway activation.