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PHD1 regulates p53-mediated colorectal cancer chemoresistance.

EMBO Mol Med. 2015; 
DeschoemaekerSofie,Di ConzaGiusy,LillaSergio,Martín-PérezRosa,MennerichDaniela,BoonLise,HendrikxStefanie,MaddocksOliver D K,MarxChristian,RadhakrishnanPraveen,PrenenHans,SchneiderMartin,MyllyharjuJohanna,KietzmannThomas,VousdenKaren H,ZanivanSara,MazzoneMassimil
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Custom Vector Construction Full-length Flag-tagged wild-type and different proline mutant forms of p53 were generated by Genscript in a lentiviral vector where p53 is under the RSV promoter as described before (Kaeser et al, 2004). Get A Quote

摘要

Overcoming resistance to chemotherapy is a major challenge in colorectal cancer (CRC) treatment, especially since the underlying molecular mechanisms remain unclear. We show that silencing of the prolyl hydroxylase domain protein PHD1, but not PHD2 or PHD3, prevents p53 activation upon chemotherapy in different CRC cell lines, thereby inhibiting DNA repair and favoring cell death. Mechanistically, PHD1 activity reinforces p53 binding to p38α kinase in a hydroxylation-dependent manner. Following p53-p38α interaction and chemotherapeutic damage, p53 can be phosphorylated at serine 15 and thus activated. Active p53 allows nucleotide excision repair by interacting with the DNA helicase XPB, thereby ... More

关键词

DNA repair,chemotherapy resistance,colorectal cancer,prolyl hydroxylase domain proteins,tumor suppressor