Isatin-Schiff base-copper (II) complex induces cell death in p53-positive tumors.
Emil R BulatovRegina SayarovaRimma MingaleevaRegina MiftakhovaMarina GomzikovaYuri IgnatyevAlexey PetukhovPavel DavidovichAlbert RizvanovNickolai A BarlevPublished in: Cell death discovery (2018)
Medicinal bioinorganic chemistry is a thriving field of drug research for cancer treatment. Transition metal complexes coordinated to essential biological scaffolds represent a highly promising class of compounds for design of novel target-specific therapeutics. We report here the biological evaluation of a novel Isatin-Schiff base derivative and its Cu(II) complex in several tumor cell lines by assessing their effects on cellular metabolism, real-time cell proliferation and induction of apoptosis. Further, the impact of compounds on the p53 protein and expression of its target genes, including MDM2, p21/CDKN1A, and PUMA was evaluated. Results obtained in this study provide further evidence in support of our prior data suggesting the p53-mediated mechanism of action for Isatin-Schiff base derivatives and their complexes and also shed light on potential use of these compounds for stimulation of apoptosis in breast cancer cells via activation of the pro-apoptotic PUMA gene.
Keyphrases
- cell death
- cell cycle arrest
- transition metal
- cell proliferation
- breast cancer cells
- oxidative stress
- genome wide
- endoplasmic reticulum stress
- poor prognosis
- pi k akt
- binding protein
- copy number
- small molecule
- cell cycle
- electronic health record
- emergency department
- machine learning
- adverse drug
- long non coding rna
- signaling pathway
- drug discovery
- metal organic framework
- drug induced
- climate change
- bioinformatics analysis