Inhibitory effects of isoliquiritigenin on the migration and invasion of human breast cancer cells

Kai Lee Wang, Shih Min Hsia, Chia Jung Chan, Full Young Chang, Chih Yang Huang, Da Tian Bau, Paulus S. Wang

Research output: Contribution to journalArticlepeer-review

60 Citations (Scopus)

Abstract

Introduction: Isoliquiritigenin (ISL) is a natural phenolic compound extracted from licorice. Previous studies have shown that ISL is a potent antioxidant with anti-inflammatory and antitumor activities. The anti-invasive activity of ISL was still unclear. The actual causes of death for most breast cancer patients were due to the tumor metastasis. Attenuating the expression of vascular endothelial growth factor (VEGF) and matrix metalloproteinases (MMPs) is well known to prevent tumor metastasis. Objectives: The purpose of this study is to investigate the effects of ISL on VEGF and MMP expression in highly metastatic human breast cancer cell line, MDA-MB-231. Results: ISL reduced the secretions and protein levels of VEGF. The VEGF upstream regulatory protein, hypoxia-inducible factor 1-alpha (HIF-1α), was also reduced after ISL treatment. Moreover, ISL inhibited the expression and gelatinolytic activity of MMP-2 and MMP-9 which were confirmed by western blot and gelatin zymography assay. Additionally, the anti-migratory activity of ISL was further confirmed by chamber migration assay and wound migration assay. Upstream signaling pathways, including the expression of phosphatidylinositol-3 kinase (PI3K), the phosphorylation of p38 and Akt kinase and NF-κB DNA binding activity, were suppressed by ISL. Conclusion: These findings suggest that ISL suppresses the migration of MDA-MB-231 cells by inhibiting the upstream signaling pathways.

Original languageEnglish
Pages (from-to)337-349
Number of pages13
JournalExpert Opinion on Therapeutic Targets
Volume17
Issue number4
DOIs
Publication statusPublished - Apr 2013

Keywords

  • Breast cancer
  • HIF-1α
  • Isoliquiritigenin
  • Migration
  • VEGF

ASJC Scopus subject areas

  • Drug Discovery
  • Pharmacology
  • Clinical Biochemistry
  • Molecular Medicine

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