Rational Design of Novel Allosteric EYA2 Inhibitors as Potential Therapeutics for Multiple Brain Cancers.
Lukas GardnerJohn RossiBrock ArmstrongMia MuseAlex LaVeckMelanie A BlevinsLingdi ZhangHeide L FordRui ZhaoXiang WangPublished in: ChemMedChem (2024)
The Eyes Absent (EYA) family of developmental proteins, often in partnership with the sine oculis (SIX) homeobox proteins, promote cancer metastasis and recurrence in numerous tumor types. In addition to being a transcriptional coactivator, EYA2 is a Tyr phosphatase that dephosphorylates H2AX which leads to repair instead of apoptosis upon DNA damage and ERβ which inhibits the anti-tumor transcriptional activity of ERβ. The SIX members of the EYA-SIX complex are difficult to target, therefore, we targeted the EYA2 to promote cell death and prevent cancer progression. We conducted structural optimization of a previously discovered allosteric inhibitor of EYA2, 9987, using the combination of in silico modeling, biochemical and cell-based assays. A new series of compounds was developed with significantly improved cellular activity and physiochemical properties desirable for brain targets. Specifically, compound 2 e showed >30-fold improvement in the medulloblastoma cell line D458, relative to 9987, while maintaining potent and selective inhibitory activity against EYA2 Tyr phosphatase activity and a good multiparameter optimization score for central nervous system drugs.
Keyphrases
- cell death
- dna damage
- small molecule
- papillary thyroid
- oxidative stress
- gene expression
- cell cycle arrest
- squamous cell
- white matter
- transcription factor
- resting state
- childhood cancer
- single cell
- estrogen receptor
- molecular docking
- mesenchymal stem cells
- high throughput
- dna repair
- cerebral ischemia
- drug delivery
- young adults
- breast cancer cells
- cell therapy
- functional connectivity
- human health
- lymph node metastasis
- free survival
- heat stress