Scholarlink

Purpose <p>The aim of this study was to investigate the function and regulatory mechanism of Interleukin-6 (IL-6) in pituitary-derived folliculostellate (PDFS) cells and to explore the mechanism of metformin against PDFS cells growth through IL-6.</p> Methods <p>Immunohistochemical staining was conducted on clinical samples from non-functioning pituitary adenomas (NFPA) patients and normal individuals to assess IL-6 and Programmed Death-Ligand 1(PD-L1) expression. PDFS cells were treated with IL-6 to evaluate their effects on cell viability, proliferation, and migration through various assays. Similar assays were performed to assess the counteractive effects of metformin, focusing on the IL-6/ERK pathway and PD-L1 expression. Western blot analysis was utilized to examine apoptosis-related proteins, and Annexin V-FITC/PI double staining was used to detect cell apoptosis. It also involves assessing the effects of metformin treatment on tumor IL-6 and PD-L1 expression, tumor size, and potential toxic side effects in PDFS xenograft mice.</p> Results <p>Clinical samples showed increased IL-6 and PD-L1 expression in NFPA compared to normal pituitary tissues. IL-6 treatment significantly enhanced PDFS cell viability(Increased by 46% within 48&#xa0;h), proliferation(Increased by 24% within 48&#xa0;h), and migration(Increased by 19% within 48&#xa0;h). Metformin treatment resulted in the downregulation of IL-6 expression and mitigated IL-6-induced effects on PDFS cells. Additionally, metformin-induced apoptosis and reduced tumor size in xenograft nude mice without observable toxic side effects.</p> Conclusion <p>Metformin downregulates the expression of IL-6 in PDFS cells, inhibits the activation of the ERK pathway, thereby suppressing cell proliferation and PD-L1 expression, and induces cell apoptosis.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Metformin induces apoptosis in pituitary-derived folliculostellate cells via the IL-6/ERK pathway

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年4月24日

查看全文
  • Xin Wang,
  • Siyuan Li,
  • Dong Fan,
  • Yuyou Luo,
  • Huitong Chen,
  • Zhongyu Wang,
  • Xingyi Yuan,
  • Jing Liu,
  • Zongming Wang

摘要

Purpose

The aim of this study was to investigate the function and regulatory mechanism of Interleukin-6 (IL-6) in pituitary-derived folliculostellate (PDFS) cells and to explore the mechanism of metformin against PDFS cells growth through IL-6.

Methods

Immunohistochemical staining was conducted on clinical samples from non-functioning pituitary adenomas (NFPA) patients and normal individuals to assess IL-6 and Programmed Death-Ligand 1(PD-L1) expression. PDFS cells were treated with IL-6 to evaluate their effects on cell viability, proliferation, and migration through various assays. Similar assays were performed to assess the counteractive effects of metformin, focusing on the IL-6/ERK pathway and PD-L1 expression. Western blot analysis was utilized to examine apoptosis-related proteins, and Annexin V-FITC/PI double staining was used to detect cell apoptosis. It also involves assessing the effects of metformin treatment on tumor IL-6 and PD-L1 expression, tumor size, and potential toxic side effects in PDFS xenograft mice.

Results

Clinical samples showed increased IL-6 and PD-L1 expression in NFPA compared to normal pituitary tissues. IL-6 treatment significantly enhanced PDFS cell viability(Increased by 46% within 48 h), proliferation(Increased by 24% within 48 h), and migration(Increased by 19% within 48 h). Metformin treatment resulted in the downregulation of IL-6 expression and mitigated IL-6-induced effects on PDFS cells. Additionally, metformin-induced apoptosis and reduced tumor size in xenograft nude mice without observable toxic side effects.

Conclusion

Metformin downregulates the expression of IL-6 in PDFS cells, inhibits the activation of the ERK pathway, thereby suppressing cell proliferation and PD-L1 expression, and induces cell apoptosis.