Silencing of protein kinase D2 induces glioma cell senescence via p53-dependent and -independent pathways.

ABSTRACT:

Background

Glioblastoma multiforme (GBM) is a highly aggressive tumor of the central nervous system with a dismal prognosis for affected patients. Aberrant protein kinase C (PKC) signaling has been implicated in gliomagenesis, and a member of the PKC-activated protein kinase D (PRKD) family, PRKD2, was identified as mediator of GBM growth in vitro and in vivo.

Methods

The outcome of PRKD2 silencing and pharmacological inhibition on glioma cell proliferation was established with different glioma cell lines. Western blotting, senescence assays, co-immunoprecipitation, fluorescence activated cell sorting, quantitative PCR, and immunofluorescence microscopy were utilized to analyze downstream signaling.

Results

RNA-interference (21-mer siRNA) and pharmacological inhibitio

SUBMITTER: Bernhart E 

PROVIDER: S-EPMC4057133 | biostudies-literature | 2014 Jul

REPOSITORIES: biostudies-literature