Oncogenic functions of hMDMX in in vitro transformation of primary human fibroblasts and embryonic retinoblasts.

ABSTRACT:

Background

In around 50% of all human cancers the tumor suppressor p53 is mutated. It is generally assumed that in the remaining tumors the wild-type p53 protein is functionally impaired. The two main inhibitors of p53, hMDM2 (MDM2) and hMDMX (MDMX/MDM4) are frequently overexpressed in wild-type p53 tumors. Whereas the main activity of hMDM2 is to degrade p53 protein, its close homolog hMDMX does not degrade p53, but it represses its transcriptional activity. Here we study the role of hMDMX in the neoplastic transformation of human fibroblasts and embryonic retinoblasts, since a high number of retinoblastomas contain elevated hMDMX levels.

Methods

We made use of an in vitro transformation model using a retroviral system of RNA interference and gene overexpression in primary

SUBMITTER: Lenos K 

PROVIDER: S-EPMC3179748 | biostudies-literature | 2011 Sep

REPOSITORIES: biostudies-literature