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Vol. 14, Issue 6, 2583-2591, June 2003
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Dipartimento di Biologia, Università Roma Tre, V. le G. Marconi, 446, I-00146 Roma
Submitted September 30, 2002;
Revised December 16, 2002;
Accepted January 30, 2003
Monitoring Editor: Keith R. Yamamoto
We reported previously in HepG2 cells that estradiol induces cell cycle
progression throughout the G1–S transition by the parallel
stimulation of both PKC-
and ERK signaling molecules. The analysis of
the cyclin D1 gene expression showed that only the MAP kinase
pathway was involved. Here, the presence of rapid/nongenomic,
estradiol-regulated, PI3K/AKT signal transduction pathway, its modulation by
the levels of the tumor suppressor PTEN, its cross-talk with the ERK pathway,
and its involvement in DNA synthesis and cyclin D1 gene promoter
activity have all been studied in HepG2 cells. 17
-Estradiol induced the
rapid and biphasic phosphorylation of AKT. These phosphorylations were
independent of each other, being the first wave of activation independent of
the estrogen receptor (ER), whereas the second was dependent on ER. Both
activations were dependent on PI3K activity; furthermore, the ERK pathway
modulated AKT phosphorylation by acting on the PTEN levels. The results showed
that the PI3K pathway, as well as ER, were strongly involved in both
G1–S progression and cyclin D1 promoter activity
by acting on its proximal region (-254 base pairs). These data indicate that
in HepG2 cells, different rapid/nongenomic estradiol-induced signal
transduction pathways modulate the multiple steps of G1–S
phase transition.
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