Loss of mutant p53 in HaCaT keratinocytes promotes cadmium-induced keratin 17 expression and cell death

CONCLUSIONS: The connection between mutant p53 in HaCaT keratinocytes and increased resistance to cadmium toxicity was demonstrated for the first time. Proteomic profiling revealed that TP53 knockout in HaCaT cells led to the activation of apoptosis regulatory circuits, redox systems, and DNA repair. In addition, our data support the involvement of keratin 17 in the regulation of DNA repair and cell death. Apparently, the induction of keratin 17 is p53-independent but may be inhibited by mutant p53.PMID:38547608 | DOI:10.1016/j.bbrc.2024.149834
Source: Biochemical and Biophysical Research communications - Category: Biochemistry Authors: Source Type: research