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IL-6 promotes metastasis and EMT of non-small cell lung cancer cells by up-regulating FGL1 via STAT3 pathway

  • 0Clinical Laboratory, Affiliated Zhongshan Hospital of Dalian University, Dalian, China.
Translational Cancer Research +

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August 12, 2025

|

August 12, 2025

View abstract on PubMed

Summary

This summary is machine-generated.

Interleukin-6 (IL-6) drives metastasis and epithelial-mesenchymal transition (EMT) in non-small cell lung cancer (NSCLC) by upregulating fibrinogen-like protein 1 (FGL1) via the STAT3 pathway.

Area Of Science

  • Oncology
  • Molecular Biology
  • Cancer Research

Background

  • Fibrinogen-like protein 1 (FGL1) is upregulated in cancers, including non-small cell lung cancer (NSCLC).
  • FGL1 influences epithelial-mesenchymal transition (EMT) in gastric cancer cells.
  • The role of the IL-6/FGL1 axis in NSCLC metastasis and EMT remains unclear.

Purpose Of The Study

  • To investigate the role of FGL1 in mediating NSCLC cell metastasis and EMT.
  • To elucidate the underlying signaling mechanisms of IL-6/FGL1 axis in NSCLC.

Main Methods

  • Analysis of TCGA and STARBASE databases for FGL1 gene expression in NSCLC.
  • In vitro experiments using Transwell assays, Western blotting, and microscopy.
  • In vivo studies utilizing FGL1-neutralizing antibodies and STAT3 inhibitors.

Main Results

  • High FGL1 expression correlated with poor prognosis in NSCLC patients.
  • FGL1 silencing reduced NSCLC cell proliferation, migration, and EMT.
  • IL-6 induced FGL1 expression and EMT via the STAT3 pathway; STAT3 inhibition blocked this effect.

Conclusions

  • IL-6/FGL1 signaling axis promotes NSCLC metastasis and EMT.
  • The STAT3 pathway is crucial for IL-6-induced FGL1 expression and subsequent EMT in NSCLC.

Keywords:

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