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J Biol Chem, Vol. 273, Issue 32, 20213-20222, August 7, 1998
From the Prostatic epithelial cells and most primary
prostate tumors are dependent on androgen for growth, but how androgen
regulates cellular proliferation remains unsolved. Using poorly
understood mechanisms, recurrent tumor cells evade the androgen
requirement. We utilized androgen-dependent prostatic tumor
cells to demonstrate that androgen exerts its effect on the cell cycle
by influencing specific aspects of G1-S progression.
Androgen depletion of these cells results in early G1
arrest, characterized by reduced cyclin-dependent kinase
activity, and underphosphorylated retinoblastoma tumor suppressor
protein (RB). The reduction in kinase activity was partially attributed
to reduction of specific G1 cyclins and alternate regulation of cyclin-dependent kinase inhibitors. Using
this information, we developed a reliable assay to assess the ability
of specific G1 regulatory proteins to circumvent these
controls and promote androgen-independent growth. As expected,
inactivation of RB was required for progression through the cell cycle.
Surprisingly, overexpression of G1 cyclins, which drives RB
phosphorylation, was insufficient to promote androgen-independent cell
cycle progression. Introduction of viral oncoproteins did promote
G1-S progression in the absence of androgen, dependent on
their ability to sequester RB and related proteins. These results
provide the first evidence that multiple elements governing the
G1-S transition dictate androgen-dependent growth, and the formation of androgen-independent prostatic tumors may
be because of misregulation of these processes.
Multiple G1 Regulatory Elements Control the
Androgen-dependent Proliferation of Prostatic Carcinoma
Cells
,§, and§¶
Ludwig Institute for Cancer Research, the
§ Department of Medicine, the ¶ Center for Molecular
Genetics, and the Cancer Center, University of California at San
Diego, La Jolla, California 92093-0660
Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.
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