The APE1 redox inhibitor E3330 reduces collective cell migration of human breast cancer cells and decreases chemoinvasion and colony formation when combined with docetaxel.
Patrícia S GuerreiroEduardo CorvachoJoão G CostaNuno SaraivaAna S FernandesMatilde CastroJoana P MirandaNuno Guerreiro OliveiraPublished in: Chemical biology & drug design (2017)
The human apurinic/apyrimidinic endonuclease 1 (APE1) is an ubiquitous multifunctional DNA repair enzyme and a redox signalling protein. Our work addressed the inhibition of APE1 redox function using E3330, as single agent or in combination with docetaxel (DTX), in human breast cancer MDA-MB-231 cells. E3330 decreased the colony formation of DTX-treated cells. In addition, E3330 alone significantly reduced the collective cell migration as assessed by the wound-healing assay, whereas the combined treatment decreased chemoinvasion. These results suggest that the inhibition of APE1 redox function might have therapeutic potential by modulating cell migration and invasion in metastatic breast cancer.
Keyphrases
- cell migration
- dna repair
- endothelial cells
- breast cancer cells
- induced apoptosis
- cell cycle arrest
- induced pluripotent stem cells
- metastatic breast cancer
- pluripotent stem cells
- wound healing
- stem cells
- squamous cell carcinoma
- single cell
- oxidative stress
- small molecule
- electron transfer
- mesenchymal stem cells
- young adults
- radiation therapy
- amino acid
- protein protein
- rectal cancer