Interleukin-37 mediates the anti-oral tumor activity in oral cancer through STAT3

Oral cancer constitutes a significant public health challenge, and gaining insights into the pathogenesis of oral cancer is crucial for the development of innovative therapeutic approaches. To address this objective, this study investigates the impact of interleukin-37 (IL-37) on oral cancer and its underlying mechanisms. Two oral cancer cell lines, HN13 and HSC-6, were employed in the study. Our findings reveal that IL-37 markedly inhibits cell viability and induces apoptosis in oral cancer cells. IL-37 attenuates the proliferation of oral cancer cells induced by lipopolysaccharide and tumor necrosis factor-alpha, while knockdown of <i>IL-37</i> exacerbates this induction. Furthermore, IL-37 demonstrates anti-inflammatory effects on oral cancer cells. The modulation of inflammation, proliferation, apoptosis, and migration by IL-37 is mediated through the STAT3 pathway. The outcomes of this study contribute valuable insights to a deeper understanding of oral cancer pathogenesis and pave the way for the development of novel drugs for the treatment of this disease.

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Publication Details

Journal
Open Medicine
Published
2025-01-01
DOI
https://doi.org/10.1515/med-2025-1173
Primary Topic
Cytokine Signaling Pathways and Interactions
Type
article
Field-Weighted Citation Impact
0.00
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article

Interleukin-37 mediates the anti-oral tumor activity in oral cancer through STAT3

Kunshan Li, Liyuan Zhang, Jing Zhang, Ying Zhang et al.
Open Medicine
Cytokine Signaling Pathways and Interactions
article

Interleukin-37 mediates the anti-oral tumor activity in oral cancer through STAT3

Kunshan Li, Liyuan Zhang, Jing Zhang, Ying Zhang, Yifan Wang, Jing Fang
article en

Abstract

Oral cancer constitutes a significant public health challenge, and gaining insights into the pathogenesis of oral cancer is crucial for the development of innovative therapeutic approaches. To address this objective, this study investigates the impact of interleukin-37 (IL-37) on oral cancer and its underlying mechanisms. Two oral cancer cell lines, HN13 and HSC-6, were employed in the study. Our findings reveal that IL-37 markedly inhibits cell viability and induces apoptosis in oral cancer cells. IL-37 attenuates the proliferation of oral cancer cells induced by lipopolysaccharide and tumor necrosis factor-alpha, while knockdown of <i>IL-37</i> exacerbates this induction. Furthermore, IL-37 demonstrates anti-inflammatory effects on oral cancer cells. The modulation of inflammation, proliferation, apoptosis, and migration by IL-37 is mediated through the STAT3 pathway. The outcomes of this study contribute valuable insights to a deeper understanding of oral cancer pathogenesis and pave the way for the development of novel drugs for the treatment of this disease.

Open MedicineVol. 20(1)
Hebei Medical University (CN), Fourth Hospital of Hebei Medical University (CN), First Hospital of Shijiazhuang (CN), Affiliated Hospital of Hebei University (CN), First Hospital of Qinhuangdao (CN)
Good health and well-being
Openalex Percentile: Top 83%
Cytokine Signaling Pathways and Interactions
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