Lipoic acid-induced oxidative stress abrogates IGF-1R maturation by inhibiting the CREB/furin axis in breast cancer cell lines

Oncogene. 2020 Apr;39(17):3604-3610. doi: 10.1038/s41388-020-1211-x. Epub 2020 Feb 14.

Abstract

The beneficial effects of lipoic acid (LA) in cancer treatment have been well documented in the last decade. Indeed, LA exerts crucial antiproliferative effects by reducing breast cancer cell viability, cell cycle progression and the epithelial-to-mesenchymal transition (EMT). However, the mechanisms of action (MOA) underlying these antiproliferative effects remain to be elucidated. Recently, we demonstrated that LA decreases breast cancer cell proliferation by inhibiting IGF-1R maturation via the downregulation of the proprotein convertase furin. The aim of the present study was to investigate the MOA by which LA inhibits furin expression in estrogen receptor α (ERα) (+) and (-) breast cancer cell lines. We unveil that LA exerts a pro-oxidant effect on these cell lines, the resulting reactive oxygen species (ROS) generated being responsible for the reduction in the expression of the major (CREB) protein. This transcription factor is overexpressed in many types of cancers and regulates the expression of furin in breast cancer cells independently of ERα, as evidenced herein by the inhibition of furin expression following CREB silencing. Consequently, our findings expose for the first time the complete MOA of LA via the CREB/furin axis leading to inhibition of breast cancer cell proliferation.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Breast Neoplasms / drug therapy
  • Breast Neoplasms / metabolism*
  • Breast Neoplasms / pathology
  • Cyclic AMP Response Element-Binding Protein / metabolism*
  • Female
  • Furin / metabolism*
  • Humans
  • MCF-7 Cells
  • Neoplasm Proteins / metabolism*
  • Oxidative Stress / drug effects*
  • Receptor, IGF Type 1 / metabolism*
  • Thioctic Acid / pharmacology*

Substances

  • CREB1 protein, human
  • Cyclic AMP Response Element-Binding Protein
  • IGF1R protein, human
  • Neoplasm Proteins
  • Thioctic Acid
  • Receptor, IGF Type 1
  • FURIN protein, human
  • Furin