α-Lipoic acid inhibits the migration and invasion of breast cancer cells through inhibition of TGFβ signaling

Life Sci. 2018 Aug 15:207:15-22. doi: 10.1016/j.lfs.2018.05.039. Epub 2018 May 23.

Abstract

Aims: Invasion and metastasis are the main cause of mortality in breast cancer. Hence, novel therapeutic interventions with high specificity toward invasion and metastasis are necessary. α-Lipoic acid showed antiproliferative and cytotoxic effects on several cancers including breast cancer. However, the effect of lipoic acid on breast cancer metastasis remains unclear.

Main methods: In the present study, we examined the effects of lipoic acid on the migration and invasion of MDA-MB-231 and 4T1 breast cancer cells.

Key findings: Our data showed that lipoic acid effectively inhibited the colony forming ability of highly invasive MDA-MB-231 and 4T1 cells. Moreover, the nontoxic concentrations of lipoic acid significantly reduced the migration of breast cancer cells. Lipoic acid also inhibited the TGFβ-induced angiopoietin-like 4 (ANGPTL4) expression and reduced the activity of matrix metalloproteinase-9 (MMP-9), an enzyme involved in invasion and metastasis, in both the cell lines. The inhibition of cell migration by lipoic acid is accompanied by the downregulation of FAK, ERK1/2 and AKT phosphorylation, and inhibition of nuclear translocation of β-catenin.

Significance: Our data demonstrated that lipoic acid inhibited the migration and invasion of metastatic breast cancer cells at least in part through inhibiting ERK1/2 and AKT signaling. Thus, our findings show that the inhibition of TGFβ signaling is a potential mechanism for the anti-invasive effects of lipoic acid.

Keywords: Breast cancer; Lipoic acid; Matrix metalloproteinase; Migration and invasion; TGFβ.

MeSH terms

  • Active Transport, Cell Nucleus
  • Angiopoietin-Like Protein 4 / metabolism
  • Animals
  • Breast Neoplasms / drug therapy
  • Breast Neoplasms / pathology*
  • Cell Line, Tumor
  • Cell Movement
  • Cell Proliferation
  • Dose-Response Relationship, Drug
  • Female
  • Humans
  • Matrix Metalloproteinase 9 / metabolism
  • Mice
  • Neoplasm Invasiveness
  • Phosphorylation
  • Signal Transduction
  • Thioctic Acid / pharmacology*
  • Transforming Growth Factor beta1 / metabolism*

Substances

  • ANGPTL4 protein, human
  • Angiopoietin-Like Protein 4
  • Angptl4 protein, mouse
  • TGFB1 protein, human
  • Tgfb1 protein, mouse
  • Transforming Growth Factor beta1
  • Thioctic Acid
  • MMP9 protein, human
  • Matrix Metalloproteinase 9
  • Mmp9 protein, mouse