Open AccessPKCδ requires p53 for suppression of the transformed phenotype in human colon cancer cells
Author(s) -
Perlett Gianpaolo,
Marras Emanuela,
Osti Daniela,
Felici Lara,
Zaro Sabrina,
Eguileor Magda
Publication year - 2004
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/j.1582-4934.2004.tb00481.x
Subject(s) - phenotype , effector , protein kinase c , biology , suppressor , colorectal cancer , cancer research , gene isoform , null cell , cancer cell , cancer , cell culture , kinase , mutation , microbiology and biotechnology , genetics , gene
Abstract 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 p21 waf1/cip1 is an essential downstream effector of PCKδ. Our data suf‐fested that p53 might also be involved in the suppression of the neoplastic phenotype induced by PCKδ. Here we show that homozygous knockout of p53 renders the HCT116 cell line unresponsive to PKCδ overexpression. Whereas reconstitution of p53 along did not modify the morphology and growth properties of HCT116/p53 null cells, overexpression of both p53 and PKCδ induced a number of alterations indicating suppression of the transformed phe‐notype. Interestingly, PKCδ was ineffective when overexpressed in HT29 cells, a human colon cancer line charac‐terized by the Arg273His dominant‐negative mutation of p53 . Thus, our data indicate that wild‐type p53 is an essen‐tial effector of PKCδ in human colon cancer cells.