PKCδ requires p53 for suppression of the transformed phenotype in human colon cancer cells

Gianpaolo Perletti, Emanuela Marras, Daniela Osti, Lara Felici, Sabrina Zaro, Magda De Eguileor

Research output: Contribution to journalArticlepeer-review


We have previously demonstrated that the delta isoform of Protein Kinase C (PKCδ) acts as a tumor suppressor in HCT116 human colon cancer cells, and that p21waf1/cip1 is an essential downstream effector of PKCδ. Our data suggested that p53 might also be involved in the suppression of the neoplastic phenotype induced by PKCδ. Here we show that homozygous knockout of p53 renders the HCT116 cell line unresponsive to PKCδ overexpression. Whereas reconstitution of p53 alone did not modify the morphology and growth properties of HCT116/p53null cells, overexpression of both p53 and PKCδ induced a number of alterations indicating suppression of the transformed phenotype. Interestingly, PKCδ was ineffective when overexpressed in HT29 cells, a human colon cancer line characterized by the Arg273His dominant-negative mutation of p53. Thus, our data indicate that wild-type p53 is an essential effector of PKCδ in human colon cancer cells.

Original languageEnglish
Pages (from-to)563-569
Number of pages7
JournalJournal of Cellular and Molecular Medicine
Issue number4
Publication statusPublished - Oct 2004


  • Colon cancer
  • p53
  • PKC
  • Protein kinase C delta
  • Tumor suppressor

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Biochemistry


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