AI Article Synopsis
- The iron nitrosyl complex with 2-aminothiophenyl ligand reduces viability and induces cell death in HeLa cells, displaying features typical of apoptosis.
- At the concentration causing half-maximal inhibition (IC50), it decreases the levels of the NF-κB p65 protein and the expression of specific NF-κB target genes like interleukin-8 and BIRC3.
- However, it does not affect the mRNA levels of interleukin-6 or BIRC2, indicating selective suppression of certain NF-κB-related genes associated with apoptosis.
Article Abstract
NO donating iron nitrosyl complex with 2-aminothiophenyl ligand ( complex) was studied for its ability to cause cell death and affect nuclear factor kappa B (NF-κB) signaling. The complex inhibited viability of HeLa cells and induced cell death that was accompanied by loss of mitochondrial membrane potential and characteristic for apoptosis phosphatidylserine externalization. At IC50, caused decrease in nuclear content of NF-κB p65 polypeptide and mRNA expression of NF-κB target genes encoding interleukin-8 and anti-apoptotic protein BIRC3. mRNA levels of interleukin-6 and anti-apoptotic protein BIRC2 encoding genes were not affected. Our data demonstrate that NO donating iron nitrosyl complex can inhibit tumor cell viability and induce apoptosis that is preceded by impairment of NF-κB function and suppression of a subset of NF-κB target genes.
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| http://dx.doi.org/10.3390/scipharm86040046 | DOI Listing |
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