Chrysin inhibits the cell viability, induces apoptosis and modulates expression of genes related to epigenetic events in bladder cancer cells.
Ana Paula Braga LimaAndré Sacramento MeloGabriel Monteze FerreiraGlenda Nicioli da SilvaPublished in: Natural product research (2022)
This study was conducted with the aim of exploring the molecular and cellular mechanisms of action of the chrysin (natural flavonoid compound) on bladder tumour cell lines with different status of TP53 (RT4, 5637 and T24). The cells were treated with different concentrations of chrysin (20, 40, 60, 80 and 100 µM) to analyze the cell viability, nuclear division index, mutagenicity, apoptosis rates and expression of genes related to epigenetic events ( DNMT1 , HAT1 and HDAC1 ). Results showed that the treatment with chrysin reduced the cell viability and caused apoptosis, regardless TP53 . Moreover, in the TP53 -mutated cell lines, chrysin modulated the expression of the DNMT1 , HAT1 and HDAC1 epigenetic genes, which might be a plus to the death observed in the cells with p53 mutation.
Keyphrases
- cell cycle arrest
- dna methylation
- induced apoptosis
- poor prognosis
- genome wide
- endoplasmic reticulum stress
- cell death
- gene expression
- oxidative stress
- pi k akt
- spinal cord injury
- binding protein
- genome wide identification
- long non coding rna
- histone deacetylase
- genome wide analysis
- transcription factor
- urinary tract