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The potential immunotherapy effect of Ginkgolide B thwarts oral squamous cell carcinoma progression by targeting the SREBP1/KLK8/CCL22 axis

  • 0Department of Medical Research, Taichung Veterans General Hospital, Taichung, Taiwan; Experimental Animal Center, Department of Molecular Biology and Cell Research, Chang Bing Show Chwan Memorial Hospital, Changhua, Taiwan.
Phytomedicine : International Journal of Phytotherapy and Phytopharmacology +

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December 1, 2024

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December 1, 2024

View abstract on PubMed

Summary

This summary is machine-generated.

Ginkgolide B (GB) inhibits oral cancer progression by targeting the SREBP1/KLK8/CCL22 pathway, reducing immune evasion. This offers a novel therapeutic strategy for oral cancer immunotherapy.

Area Of Science

  • Oncology
  • Immunology
  • Pharmacology

Background

  • Oral cancer is a significant health concern with poor prognosis linked to regulatory T cell (Treg) infiltration.
  • Ginkgolide B (GB), known for lipid metabolism effects, has unexplored potential in oral cancer immunotherapy.

Purpose Of The Study

  • To investigate the immunotherapeutic potential of Ginkgolide B (GB) in oral cancer.
  • To elucidate the mechanisms by which GB modulates the sterol regulatory element-binding protein 1 (SREBP1)/kallikrein-related peptidase 8 (KLK8)/CC motif chemokine ligand 22 (CCL22) axis in oral cancer.

Main Methods

  • Correlation analysis of SREBP1, KLK8, and CCL22 with oral cancer prognosis using tissue arrays and GEO data.
  • RNA sequencing to assess GB's molecular effects on oral cancer cell lines (SAS, KYSE-510, TE-1).
  • In vivo, ex vivo, and in vitro assays, including electrophoretic mobility shift assays and mouse models, to evaluate GB's therapeutic efficacy and mechanism of action.

Main Results

  • SREBP1 expression negatively correlates with oral cancer prognosis, while SREBP1 and KLK8 show positive correlation.
  • GB treatment or SREBP1 knockdown inhibited oral cancer cell proliferation, migration, and Treg chemotaxis.
  • GB acts by attenuating SREBP1-regulated KLK8 transcription, thereby reducing CCL22 secretion and Treg recruitment.

Conclusions

  • Ginkgolide B (GB) functions as a novel SREBP1 inhibitor in oral cancer.
  • GB effectively combats oral cancer immune escape by modulating the SREBP1/KLK8/CCL22 axis.
  • GB presents a promising new therapeutic avenue for oral cancer immunotherapy.

Keywords:

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