HPV16 E7-dependent transformation activates NHE1 through a PKA-RhoA-induced inhibition of p38alpha.

ABSTRACT:

Background

Neoplastic transformation originates from a large number of different genetic alterations. Despite this genetic variability, a common phenotype to transformed cells is cellular alkalinization. We have previously shown in human keratinocytes and a cell line in which transformation can be turned on and followed by the inducible expression of the E7 oncogene of human papillomavirus type 16 (HPV16), that intracellular alkalinization is an early and essential physiological event driven by the up-regulation of the Na/(+)H(+) exchanger isoform 1 (NHE1) and is necessary for the development of other transformed phenotypes and the in vivo tumor formation in nude mice.

Methodology

Here, we utilize these model systems to elucidate the dynamic sequence of alterations of the up

SUBMITTER: Cardone RA 

PROVIDER: S-EPMC2568952 | biostudies-literature | 2008

REPOSITORIES: biostudies-literature