Send to

Choose Destination
See comment in PubMed Commons below
Photochem Photobiol. 2013 Jan-Feb;89(1):163-72. doi: 10.1111/j.1751-1097.2012.01215.x. Epub 2012 Sep 13.

The p53-dependent expression of frataxin controls 5-aminolevulinic acid-induced accumulation of protoporphyrin IX and photo-damage in cancerous cells.

Author information

Department of Biotechnology, Kyoto Institute of Technology, Kyoto, Japan.


Mitochondrial frataxin is involved in various functions such as iron homeostasis, iron-sulfur cluster biogenesis, the protection from oxidative stress and apoptosis and acts as a tumor suppressor protein. We now show that the expression of frataxin is stimulated in a p53-dependent manner and prove that frataxin is a direct p53 target gene by showing that the p53-responsive element in the promoter of the mouse frataxin gene is bound by p53. The bacterial expression of human frataxin stimulated maturation of human ferrochelatase, which catalyzes the insertion of iron into protoporphyrin at the last step of heme biosynthesis. Overexpression of frataxin in human cancer A431 and HeLa cells lowered 5-aminolevulinic acid(ALA)-induced accumulation of protoporphyrin and induced resistance to ALA-induced photo-damage, whereas p53 silencing with siRNA in non tumor HEK293T cells down-regulated the expression of frataxin and increased the accumulation of protoporphyrin. Thus, the decrease of the expression of frataxin unregulated by p53 in tumor cells enhances ALA-induced photo-damage, by down-regulation of mitochondrial functions.

[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Wiley
    Loading ...
    Support Center