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Advances in Brief |
Department of Molecular and Cellular Oncology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030
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ABSTRACT |
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 Top ABSTRACT IntroductionMaterials and MethodsResults and DiscussionREFERENCES |
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Introduction |
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TopABSTRACTIntroductionMaterials and MethodsResults and DiscussionREFERENCES |
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30% of human breast and ovarian cancers
(7)
. Unlike the other members of EGF receptors,
HER-2/neu has an intrinsic tyrosine kinase
activity that activates the receptor-mediated signal transduction in
the absence of ligand. Although EGF binds to an EGF receptor to induce
receptor dimerization and activate PI3K (8)
,
HER-2/neu homodimer constitutively activates the
PI3K-Akt pathway without extracellular stimulation (9)
.
Activation of PI3K generates phosphatidylinositol-3,4,5-triphosphate,
which in turn binds to the pleckstrin homology domain of
serine/threonine kinase Akt, resulting in recruitment of Akt to the
cell membrane. A conformational change of Akt follows, which enables
residues Thr-308 and Ser-473 to be phosphorylated by upstream kinases,
PDK-1 and PDK-2 or ILK, respectively (10)
. Activated Akt
phosphorylates specific targets such as Bad (11)
,
pro-caspase-9 (12)
, and transcription factor FKHRL1
(13)
at the Akt phosphorylation consensus sequence
R-X-R-X-X-S/T, thus promoting cell survival and blocking apoptosis. In
this way, the PI3K-Akt pathway plays a critical role in antiapoptosis
that may contribute to the pathogenesis of cancer (10)
. In
the present study, we examined whether Akt and HER-2/neu are
involved in the AR signaling pathway and whether they play a role in
androgen-independent survival or growth of prostate cancer cells. We
show that HER-2/neu activated Akt to promote prostate cancer
cell survival and growth in the absence of androgen. The
HER-2/neu-induced AR signaling and cell survival/growth
effects were blocked by the DN-Akt or an inhibitor LY294002. Moreover,
Akt specifically binds to AR and phosphorylates Ser-213 and Ser-791 of
AR. Thus, our findings provide a molecular mechanism for the
HER-2/neu-induced androgen-independent survival and growth
of prostate cancer cells. |
Materials and Methods |
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TopABSTRACTIntroductionMaterials and MethodsResults and DiscussionREFERENCES |
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1.5 kb)
containing the PSA promoter (640-bp) and enhancer (820-bp) into the
luc expression vector. The PRE-luc reporter (PRE-luc) contains two
copies of the progesterone/androgen response element (14)
.
For survival assays, LNCaP cells were prepared as described above and
cotransfected with 0.2 µg of CMV-luc plasmid and 2 µg of each
expression plasmid as indicated. The transfected cells were cultured in
the absence or presence of androgen as described above. The relative
survival rate (percentage of cell survival) between the cultures in the
absence and presence of androgen was determined by the luc activities
and shown as a ratio, using the activity in the medium containing
androgen as 100%. The data represent the mean value of at least three
independent experiments, and statistical significance was calculated
with the 
2
test using SPSS software.
P < 0.05 was set as the criterion for
statistical significance.
Cell Proliferation Assays.
LNCaP cells were plated the day before transfection at 50% confluence
in 100-mm dishes. The cells were cotransfected with 1.0 µg of
pDsRed1-C1 plasmid (Clontech) and 15 µg of a constitutively active
HER2/neu (HER2/neu*), the Thr-1172 of which has
been changed to Glu, or 15 µg of the control vector. After
transfection, the cells were cultured in phenol red-free medium
supplemented with 5% of c-FBS in the absence or presence of R1881 (0.1
nM). As controls, 36 h after transfection,
the transfected cells were treated with 40 µM
of LY294002 (Biomol), which is an inhibitor for the PI3K/Akt pathway.
For BrdUrd labeling, 48 h after transfection, the cells were
incubated with BrdUrd (10 µM) for 1 h. The
transfected cells expressing the red fluorescent protein were selected
by fluorescence-activated cell sorter and plated onto
poly-L-lysine-coated slides using Cytospin II.
The BrdUrd-labeled cells were detected using a BrdUrd labeling and
detection kit (Roche) and evaluated under a fluorescent microscope. The
percentages of BrdUrd-labeled cells were calculated based on
400–800 RFP+ cells from each sample.
Immunoprecipitation, Western Blot, and Immunocomplex Kinase
Assays.
LNCaP cells were washed with PBS, lysed in ice-cold RIPA buffer
containing protease inhibitors, and centrifuged at 14,000 x g for 10 min at 4°C. For immunoprecipitation, 1 mg
of each supernatant (cell lysate) was incubated with an anti-AR mAb
(Pharmingen) or mouse IgG (negative control) overnight at 4°C. Then,
protein G-agarose (Roche) was added and incubated for 2 h at 4°C
with rotation. The immunocomplex was recovered by centrifugation,
washed four times with lysis buffer, dissolved in loading buffer, and
subjected to SDS-PAGE. For Western blot, the protein samples were
subjected to SDS-PAGE and transferred onto nitrocellulose membranes.
The membranes were blocked with 5% nonfat dry milk in PBS containing
0.05% Tween 20 and incubated with an anti-p-Akt (S-473) antibody (New
England Biolabs) and then with horseradish peroxidase-conjugated
secondary antibodies according to the manufacturer’s instructions. The
immunoblots were visualized by an enhanced chemiluminescence kit (ECL;
Amersham). Immunocomplex kinase assays were performed as described
previously (15)
. Specifically, 293T cells were transfected
with the HA-tagged CA-Akt expression plasmid, the cells were harvested,
and whole-cell lysates were prepared 48 h after transfection.
After immunoprecipitation with an anti-HA mAb, phosphorylation of AR
was determined by an immunocomplex kinase assay, using wt or mut
GST-AR-N or GST-AR-C or histone 2B (Roche) as substrates. The GST-AR-N
and GST-AR-C plasmids were constructed by subcloning of the cDNA
fragments containing the N- or COOH-terminal domain of AR (AR-N or
AR-C) by the PCR technique. The mutant GST-AR-N and GST-AR-C were
generated by site-directed mutagenesis using specific oligonucleotides
and a QuickChange site-directed mutagenesis kit (Stratagene) to change
the Ser-213 and Ser-791 residues to Ala-213 and Ala-791, respectively.
The GST-fusion proteins were purified by affinity chromatography
on glutathione-Sepharose 4B (Amersham).
Pull-Down Assays.
293T cells were transfected with the HA-tagged CA-Akt expression
plasmid, the cells were harvested, and whole-cell lysates were prepared
48 h after transfection. Fifty µl of glutathione-Sepharose were
incubated with 90 µg of GST-AR-N or GST-AR-C or GST protein for
3 h and washed with washing buffer [50 mM Tris-HCl
(pH 8.0), 150 mM NaCl, and 0.5% NP40] three times. The
293T cell lysates were mixed with the GST-AR-N or GST-AR-C or GST
conjugated glutathione-Sepharose, incubated overnight at 4°C, and
washed three times with washing buffer. The proteins bound to the
GST-AR-N or GST-AR-C or GST-conjugated glutathione-Sepharose were
analyzed by Western blotting using an anti-HA mAb (12CA5).
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Results and Discussion |
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TopABSTRACTIntroductionMaterials and MethodsResults and DiscussionREFERENCES |
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2-fold (Fig. 1a)
,
suggesting that Akt activates PSA transcription. To compare the
transactivation activity of Akt in the absence and presence of the
hormone, we carried out the same DNA transfection experiments as
described above, except that the cells were cultured in phenol red-free
medium supplemented with the charcoal-treated serum to allow precise
control of the concentration of androgen. In the absence of androgen,
CA-Akt stimulated the PSA-luc reporter 5-fold (Fig. 1b
,
Lane 4 versus Lane 1), and DN-Akt inhibited the reporter
2-fold (Fig. 1b
, Lane 7 versus Lane 1),
suggesting that Akt can activate the PSA promoter/enhancer in the
absence of androgen. Consistent with this concept, PTEN, which is a
well-known PI3K/Akt inhibitor, also blocked activation of the PSA
promoter/enhancer (Fig. 1
b, Lanes 10–12) in the absence or
presence of androgen, further suggesting that the Akt pathway may be
required for transactivation of the PSA promoter/enhancer. Moreover,
the PSA transcriptional activity induced by CA-Akt in the absence of
R1881 (Fig. 1b
, Lane 4 versus Lane 1) is slightly
stronger than that stimulated by R1881 alone (Fig. 1b
,
Lane 3 versus Lane 1); activation of PSA transcription
appears to be less effective by R1881 in the presence of CA-Akt
(1.6-fold; Fig. 1b
, Lane 6 versus Lane 4) than
in the absence of CA-Akt (4-fold; Fig. 1b
, Lane 3
versus Lane 1). Taken together, these results imply that Akt is
involved in androgen-independent transactivation function.
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2-fold in the absence of the hormone, whereas DN-Akt failed to
increase LNCaP cell survival (Fig. 1c)
. The relative
survival rate (percentage of cell survival) was shown as a ratio
between the survival of LNCaP cells in the absence and presence of
androgen. To confirm that this Akt effect is independent of androgen,
we performed similar DNA transfection experiments and cultured the
cells in phenol red-free medium supplemented with the charcoal-treated
serum with or without R1881. CA-Akt significantly increased LNCaP cell
survival in the absence of R1881, whereas DN-Akt and PTEN decreased
LNCaP cell survival in the absence of R1881 (Fig. 1d)
. Our
data further support the notion that Akt mediates androgen-independent
transactivation function and suggest that Akt may enhance prostate
cancer cell survival during androgen deprivation.
Because HER-2/neu has been shown recently to activate AR
signaling (9
, 10)
and we have demonstrated previously that
HER-2/neu activates the Akt pathway, we determined whether
Akt may be involved in the HER-2/neu-activated AR signaling.
We cotransfected LNCaP cells with the PSA-luc reporter and an activated
form of HER-2/neu (HER-2/neu*) or
HER-2/neu* plus DN-Akt and cultured the cells in the
hormone-free medium as described above. HER-2/neu* activated
the PSA promoter/enhancer 8-fold (Fig. 2
a, Lane 5 versus Lane 2, at
0.1 nM R1881) or 5-fold (Fig. 2
a, Lane 6 versus Lane 3, at
1.0 nM R1881) in the presence of R1881, and
10-fold (Fig. 2
a, Lane 4 versus
Lane 1) in the absence of R1881. However, this stimulatory effect
of HER-2/neu* was dramatically reduced by DN-Akt or an Akt
inhibitor LY294002 (Fig. 2a)
, suggesting that activation of
the AR pathway by HER-2/neu requires functional Akt. The
PSA-luc reporter construct encodes 1400 bp of sequence consisting of a
high-affinity androgen responsive element in the promoter and an
androgen responsive region in an upstream enhancer (16
, 17)
. To exclude the possibility that some other promoter or
enhancer elements may attribute to PSA activation by androgen, we
further analyzed the PRE-luc reporter, which contains two copies of
high-affinity androgen response element (14)
. Similarly,
HER-2/neu* activated the PRE-luc reporter significantly in
the presence or absence of R1881. However, this stimulatory effect was
blocked by DN-Akt (data not shown), confirming that
HER-2/neu activates AR signaling via the Akt pathway.
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30%) of LNCaP cells in the absence of R1881,
whereas this enhancing effect by HER-2/neu* was abolished by
DN-Akt (Fig. 2b)
. These results suggest that
HER-2/neu promotes prostate cancer cell survival upon
androgen withdrawal through the Akt pathway. Furthermore, to examine
whether HER-2/neu can stimulate prostate cancer cell
proliferation during androgen withdrawal, we measured the DNA synthesis
rate by the BrdUrd incorporation rate. We cotransfected LNCaP cells
with a red fluorescent protein expression vector pDsRed1-C1 and
HER-2/neu* or an empty vector and cultured the cells in the
hormone-free medium with or without R1881. In addition, one set of the
HER-2/neu*-transfected cells were treated with LY294002.
Subsequently, the red fluorescence-positive cells were sorted, plated
on slides by cytospin, and assayed for proliferation by BrdUrd
incorporation. Significantly, HER-2/neu* augmented the
BrdUrd incorporation rate (i.e., growth rate) of LNCaP cells
2-fold (Lane 3 versus Lane 1) in the absence of R1881 and
1.5-fold (Lane 4 versus Lane 2) in the presence of R1881
(Fig. 2c)
. Representative fluorescent pictures are shown
(Fig. 2d)
. However, this growth-stimulatory effect of
HER-2/neu* was strongly blocked by LY294002 (Fig. 2c)
, confirming that activation of the androgen-independent
growth by HER-2/neu requires a functional PI3-K/Akt pathway.
Taken together, HER-2/neu promotes prostate cancer cell
survival and growth upon androgen deprivation via the Akt pathway.
Because Akt can activate the AR pathway, we investigated whether the
interactions between Akt and AR can occur in vivo.
Whole-cell lysates of LNCaP cells were immunoprecipitated using an
anti-AR mAb or mouse IgG, and the immunoprecipitated proteins were
subjected to Western blotting using an antibody against phosphorylated
Akt (p-Akt). Our results showed that p-Akt (activated Akt) was
coimmunoprecipitated with an mAb against AR but not with the control
IgG (Fig. 3a)
, suggesting that
the endogenous AR is specifically associated with activated Akt
in vivo. Comparison of the amino acid sequences of AR among
human, rat, and mouse reveals two conserved putative consensus Akt
phosphorylation sites, Ser-213 and Ser-791, based on the human sequence
(Fig. 3b)
. Therefore, we examined which sites of the AR
protein can interact with CA-Akt in vitro. We generated and
purified GST-fusion proteins containing the
NH2-terminal half of AR (designated GST-AR-N) and
the COOH-terminal portion of AR (designated GST-AR-C), where Ser-213
and Ser-791 residues reside in AR-N and AR-C, respectively. Whole-cell
lysates of HA-CA-Akt transfected 293T cells were incubated with
glutathione-Sepharose preloaded with either GST-AR-N or GST-AR-C or GST
protein. The bound proteins were eluted and immunoblotted with an
anti-HA mAb. Specific Mr 62,000 HA-Akt
proteins were detected in the GST-AR-N- and GST-AR-C-bound fractions as
well as in the total lysates (positive control) but not in the GST
(negative control) bound fractions (Fig. 3c)
. These results
suggest that both domains (Akt phosphorylation sites) of the AR protein
are specifically associated with CA-Akt protein in vitro.
Furthermore, we determined whether these two Akt target sites can be
phosphorylated by CA-Akt, using immunocomplex kinase assays. To test
the specificities of Akt phosphorylation, these two Ser-213 and Ser-791
residues within GST-AR-N and GST-AR-C were mutated to Ala residues,
designated GST-AR-N/mut and GST-AR-C/mut, respectively. To produce
CA-Akt, 293T cells were transiently transfected with HA-CA-Akt.
Whole-cell lysates of the transfected cells were immunoprecipitated
using an anti-HA mAb, and the immunoprecipitated proteins were
subjected to immunocomplex kinase assays using GST-AR-N (wt or mut) and
GST-AR-C (wt or mut) as substrates. Phosphorylation of GST-AR-N/wt and
GST-AR-C/wt was readily detected, whereas phosphorylation of
GST-AR-N/mut and GST-AR-C/mut was not detectable (Fig. 3d)
,
suggesting that Ser-213 and Ser-791 were specifically phosphorylated by
CA-Akt. As a positive control, the same immunoprecipitated proteins
were subjected to an immunocomplex kinase assay using histone 2B as a
substrate (Fig. 3e)
. As shown in Fig. 4
, a model is depicted to illustrate the
proposed parallel cell survival and proliferation pathways induced by
HER-2/neu via the Akt pathway from the current study or the
MAP kinase pathway as well reported previously (4
, 5)
. To
our knowledge, this is the first evidence that HER-2/neu
activates AR via the Akt pathway and may provide an interpretation of
how HER-2/neu can restore AR signaling to prostate cancer
cells during androgen ablation. The effect of Ser-213 and Ser-791
mutants on AR function and response to HER-2/neu-Akt
activation deserves further investigation and may open an alternative
avenue for understanding the molecular mechanism of the
androgen-independent survival and growth of prostate cancer cells. It
may lead to a new direction for developing novel anticancer therapies
for the androgen-refractory prostate cancers.
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FOOTNOTES |
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1 This work was supported by Grants R01-CA58880
and R01-CA77858 and Cancer Core Grant 16672 from the National Cancer
Institute, by the Nellie Connally Breast Cancer Research Fund, and by
the Faculty Achievement Award at M. D. Anderson Cancer Center (to
M-C. H.). Y. W. and K. M. are predoctoral and postdoctoral fellows,
respectively, supported by United States Army Breast Cancer Research
Training Grant DMAD 17-99-1-9264). 
2 These authors contributed equally to this
work.
3 To whom requests for reprints should be
addressed, at Department of Molecular and Cellular Oncology, Box 108,
The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe
Boulevard, Houston, TX 77030. Phone: (713) 792-3668; Fax:
(713) 794-4784; E-mail: mhung{at}notes.mdacc.tmc.edu
4 The abbreviations used are: AR, androgen
receptor; PSA, prostate-specific antigen; MAP, mitogen-activated
protein; EGF, epidermal growth factor; PI3K, phosphatidylinositol
3-kinase; HA, hemagglutinin; CMV, cytomegalovirus; mAb, monoclonal
antibody; ß-gal, ß-galactosidase; c-FBS, charcoal-treated FBS;
BrdUrd, bromodeoxyuridine; wt, wild type; mut, mutant; GST,
glutathione S-transferase; RFP, red fluorescent protein;
luc, luciferase; DN-Akt, dominant-negative Akt; CA-Aft, constitutively
active Akt.
Received 7/19/00. Accepted 10/31/00.
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REFERENCES |
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L. S. Lyons and K. L. Burnstein Vav3, a Rho GTPase Guanine Nucleotide Exchange Factor, Increases during Progression to Androgen Independence in Prostate Cancer Cells and Potentiates Androgen Receptor Transcriptional Activity Mol. Endocrinol., May 1, 2006; 20(5): 1061 - 1072. [Abstract] [Full Text] [PDF]
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Z. Zheng, C. Cai, J. Omwancha, S.-Y. Chen, T. Baslan, and L. Shemshedini SUMO-3 Enhances Androgen Receptor Transcriptional Activity through a Sumoylation-independent Mechanism in Prostate Cancer Cells J. Biol. Chem., February 17, 2006; 281(7): 4002 - 4012. [Abstract] [Full Text] [PDF]
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S. S. Taneja, S. Ha, N. K. Swenson, H. Y. Huang, P. Lee, J. Melamed, E. Shapiro, M. J. Garabedian, and S. K. Logan Cell-specific Regulation of Androgen Receptor Phosphorylation in Vivo J. Biol. Chem., December 9, 2005; 280(49): 40916 - 40924. [Abstract] [Full Text] [PDF]
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 S. Veeramani, T.-C. Yuan, S.-J. Chen, F.-F. Lin, J. E Petersen, S. Shaheduzzaman, S. Srivastava, R. G MacDonald, and M.-F. Lin Cellular prostatic acid phosphatase: a protein tyrosine phosphatase involved in androgen-independent proliferation of prostate cancer Endocr. Relat. Cancer, December 1, 2005; 12(4): 805 - 822. [Abstract] [Full Text] [PDF]
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N. P. Mahajan, Y. E. Whang, J. L. Mohler, and H. S. Earp Activated Tyrosine Kinase Ack1 Promotes Prostate Tumorigenesis: Role of Ack1 in Polyubiquitination of Tumor Suppressor Wwox Cancer Res., November 15, 2005; 65(22): 10514 - 10523. [Abstract] [Full Text] [PDF]
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H. I. Scher and C. L. Sawyers Biology of Progressive, Castration-Resistant Prostate Cancer: Directed Therapies Targeting the Androgen-Receptor Signaling Axis J. Clin. Oncol., November 10, 2005; 23(32): 8253 - 8261. [Abstract] [Full Text] [PDF]
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L. Yang, S. Xie, Md. S. Jamaluddin, S. Altuwaijri, J. Ni, E. Kim, Y.-T. Chen, Y.-C. Hu, L. Wang, K.-H. Chuang, et al. Induction of Androgen Receptor Expression by Phosphatidylinositol 3-Kinase/Akt Downstream Substrate, FOXO3a, and Their Roles in Apoptosis of LNCaP Prostate Cancer Cells J. Biol. Chem., September 30, 2005; 280(39): 33558 - 33565. [Abstract] [Full Text] [PDF]
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L. Chen, S. Meng, H. Wang, P. Bali, W. Bai, B. Li, P. Atadja, K. N. Bhalla, and J. Wu Chemical ablation of androgen receptor in prostate cancer cells by the histone deacetylase inhibitor LAQ824 Mol. Cancer Ther., September 1, 2005; 4(9): 1311 - 1319. [Abstract] [Full Text] [PDF]
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S. Gao, P. Lee, H. Wang, W. Gerald, M. Adler, L. Zhang, Y.-F. Wang, and Z. Wang The Androgen Receptor Directly Targets the Cellular Fas/FasL-Associated Death Domain Protein-Like Inhibitory Protein Gene to Promote the Androgen-Independent Growth of Prostate Cancer Cells Mol. Endocrinol., July 1, 2005; 19(7): 1792 - 1802. [Abstract] [Full Text] [PDF]
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Z Culig, H Steiner, G Bartsch, and A Hobisch Mechanisms of endocrine therapy-responsive and -unresponsive prostate tumours Endocr. Relat. Cancer, June 1, 2005; 12(2): 229 - 244. [Abstract] [Full Text] [PDF]
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T.-C. Tsai, Y.-L. Lee, W.-C. Hsiao, Y.-P. Tsao, and S.-L. Chen NRIP, a Novel Nuclear Receptor Interaction Protein, Enhances the Transcriptional Activity of Nuclear Receptors J. Biol. Chem., May 20, 2005; 280(20): 20000 - 20009. [Abstract] [Full Text] [PDF]
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 I. M. Ghobrial, T. E. Witzig, and A. A. Adjei Targeting Apoptosis Pathways in Cancer Therapy CA Cancer J Clin, May 1, 2005; 55(3): 178 - 194. [Abstract] [Full Text] [PDF]
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Y. Liu, S. Majumder, W. McCall, C. I. Sartor, J. L. Mohler, C. W. Gregory, H. S. Earp, and Y. E. Whang Inhibition of HER-2/neu Kinase Impairs Androgen Receptor Recruitment to the Androgen Responsive Enhancer Cancer Res., April 15, 2005; 65(8): 3404 - 3409. [Abstract] [Full Text] [PDF]
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B. Cinar, A. De Benedetti, and M. R. Freeman Post-Transcriptional Regulation of the Androgen Receptor by Mammalian Target of Rapamycin Cancer Res., April 1, 2005; 65(7): 2547 - 2553. [Abstract] [Full Text] [PDF]
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X. Liao, S. Tang, J. B. Thrasher, T. L. Griebling, and B. Li Small-interfering RNA-induced androgen receptor silencing leads to apoptotic cell death in prostate cancer Mol. Cancer Ther., April 1, 2005; 4(4): 505 - 515. [Abstract] [Full Text] [PDF]
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T.-L. Cha, L. Qiu, C.-T. Chen, Y. Wen, and M.-C. Hung Emodin Down-Regulates Androgen Receptor and Inhibits Prostate Cancer Cell Growth Cancer Res., March 15, 2005; 65(6): 2287 - 2295. [Abstract] [Full Text] [PDF]
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P. M Ghosh, S. N Malik, R. G Bedolla, Y. Wang, M. Mikhailova, T. J Prihoda, D. A Troyer, and J. I Kreisberg Signal transduction pathways in androgen-dependent and -independent prostate cancer cell proliferation Endocr. Relat. Cancer, March 1, 2005; 12(1): 119 - 134. [Abstract] [Full Text] [PDF]
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G. Han, G. Buchanan, M. Ittmann, J. M. Harris, X. Yu, F. J. DeMayo, W. Tilley, and N. M. Greenberg Mutation of the androgen receptor causes oncogenic transformation of the prostate PNAS, January 25, 2005; 102(4): 1151 - 1156. [Abstract] [Full Text] [PDF]
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 J. Choi, A. M. Miller, M. J. Nolan, B. Y. J. T. Yue, S. T. Thotz, A. F. Clark, N. Agarwal, and P. A. Knepper Soluble CD44 Is Cytotoxic to Trabecular Meshwork and Retinal Ganglion Cells In Vitro Invest. Ophthalmol. Vis. Sci., January 1, 2005; 46(1): 214 - 222. [Abstract] [Full Text] [PDF]
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M. Verras, J. Brown, X. Li, R. Nusse, and Z. Sun Wnt3a Growth Factor Induces Androgen Receptor-Mediated Transcription and Enhances Cell Growth in Human Prostate Cancer Cells Cancer Res., December 15, 2004; 64(24): 8860 - 8866. [Abstract] [Full Text] [PDF]
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W. H. Dragowska, C. Warburton, D. T.T. Yapp, A. I. Minchinton, Y. Hu, D. N. Waterhouse, K. Gelmon, K. Skov, J. Woo, D. Masin, et al. HER-2/neu Overexpression Increases the Viable Hypoxic Cell Population within Solid Tumors without Causing Changes in Tumor Vascularization Mol. Cancer Res., November 1, 2004; 2(11): 606 - 619. [Abstract] [Full Text] [PDF]
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H. I Scher, G. Buchanan, W. Gerald, L. M Butler, and W. D Tilley Targeting the androgen receptor: improving outcomes for castration-resistant prostate cancer Endocr. Relat. Cancer, September 1, 2004; 11(3): 459 - 476. [Abstract] [Full Text] [PDF]
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C. N. Papandreou and C. J. Logothetis Bortezomib as a Potential Treatment for Prostate Cancer Cancer Res., August 1, 2004; 64(15): 5036 - 5043. [Abstract] [Full Text] [PDF]
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L. Wang, H.-K. Lin, Y.-C. Hu, S. Xie, L. Yang, and C. Chang Suppression of Androgen Receptor-mediated Transactivation and Cell Growth by the Glycogen Synthase Kinase 3{beta} in Prostate Cells J. Biol. Chem., July 30, 2004; 279(31): 32444 - 32452. [Abstract] [Full Text] [PDF]
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D. Cheng, N. Yadav, R. W. King, M. S. Swanson, E. J. Weinstein, and M. T. Bedford Small Molecule Regulators of Protein Arginine Methyltransferases J. Biol. Chem., June 4, 2004; 279(23): 23892 - 23899. [Abstract] [Full Text] [PDF]
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 X. Liao, J. B. Thrasher, J. Holzbeierlein, S. Stanley, and B. Li Glycogen Synthase Kinase-3{beta} Activity Is Required for Androgen-Stimulated Gene Expression in Prostate Cancer Endocrinology, June 1, 2004; 145(6): 2941 - 2949. [Abstract] [Full Text] [PDF]
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T. R. Salas, J. Kim, F. Vakar-Lopez, A. L. Sabichi, P. Troncoso, G. Jenster, A. Kikuchi, S.-Y. Chen, L. Shemshedini, M. Suraokar, et al. Glycogen Synthase Kinase-3{beta} Is Involved in the Phosphorylation and Suppression of Androgen Receptor Activity J. Biol. Chem., April 30, 2004; 279(18): 19191 - 19200. [Abstract] [Full Text] [PDF]
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 C. A. Heinlein and C. Chang Androgen Receptor in Prostate Cancer Endocr. Rev., April 1, 2004; 25(2): 276 - 308. [Abstract] [Full Text] [PDF]
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C. Warburton, W. H. Dragowska, K. Gelmon, S. Chia, H. Yan, D. Masin, T. Denyssevych, A. E. Wallis, and M. B. Bally Treatment of HER-2/neu Overexpressing Breast Cancer Xenograft Models with Trastuzumab (Herceptin) and Gefitinib (ZD1839): Drug Combination Effects on Tumor Growth, HER-2/neu and Epidermal Growth Factor Receptor Expression, and Viable Hypoxic Cell Fraction Clin. Cancer Res., April 1, 2004; 10(7): 2512 - 2524. [Abstract] [Full Text] [PDF]
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C. W. Gregory, X. Fei, L. A. Ponguta, B. He, H. M. Bill, F. S. French, and E. M. Wilson Epidermal Growth Factor Increases Coactivation of the Androgen Receptor in Recurrent Prostate Cancer J. Biol. Chem., February 20, 2004; 279(8): 7119 - 7130. [Abstract] [Full Text] [PDF]
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H.-K. Lin, Y.-C. Hu, L. Yang, S. Altuwaijri, Y.-T. Chen, H.-Y. Kang, and C. Chang Suppression Versus Induction of Androgen Receptor Functions by the Phosphatidylinositol 3-Kinase/Akt Pathway in Prostate Cancer LNCaP Cells with Different Passage Numbers J. Biol. Chem., December 19, 2003; 278(51): 50902 - 50907. [Abstract] [Full Text] [PDF]
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 L. Li, C. H. Ren, S. A. Tahir, C. Ren, and T. C. Thompson Caveolin-1 Maintains Activated Akt in Prostate Cancer Cells through Scaffolding Domain Binding Site Interactions with and Inhibition of Serine/Threonine Protein Phosphatases PP1 and PP2A Mol. Cell. Biol., December 15, 2003; 23(24): 9389 - 9404. [Abstract] [Full Text] [PDF]
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R. Enmon, W.-H. Yang, A. M. Ballangrud, D. B. Solit, G. Heller, N. Rosen, H. I. Scher, and G. Sgouros Combination Treatment with 17-N-Allylamino-17-Demethoxy Geldanamycin and Acute Irradiation Produces Supra-Additive Growth Suppression in Human Prostate Carcinoma Spheroids Cancer Res., December 1, 2003; 63(23): 8393 - 8399. [Abstract] [Full Text] [PDF]
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A. C. Rigas, D. M. Ozanne, D. E. Neal, and C. N. Robson The Scaffolding Protein RACK1 Interacts with Androgen Receptor and Promotes Cross-talk through a Protein Kinase C Signaling Pathway J. Biol. Chem., November 14, 2003; 278(46): 46087 - 46093. [Abstract] [Full Text] [PDF]
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C. Woodham, L. Birch, and G. S. Prins Neonatal Estrogen Down-Regulates Prostatic Androgen Receptor through a Proteosome-Mediated Protein Degradation Pathway Endocrinology, November 1, 2003; 144(11): 4841 - 4850. [Abstract] [Full Text] [PDF]
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J. Edwards, N. S. Krishna, C. J. Witton, and J. M. S. Bartlett Gene Amplifications Associated with the Development of Hormone-Resistant Prostate Cancer Clin. Cancer Res., November 1, 2003; 9(14): 5271 - 5281. [Abstract] [Full Text] [PDF]
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K. Song, S. C. Cornelius, M. Reiss, and D. Danielpour Insulin-like Growth Factor-I Inhibits Transcriptional Responses of Transforming Growth Factor-{beta} by Phosphatidylinositol 3-Kinase/Akt-dependent Suppression of the Activation of Smad3 but Not Smad2 J. Biol. Chem., October 3, 2003; 278(40): 38342 - 38351. [Abstract] [Full Text] [PDF]
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M. Letsch, A. V. Schally, K. Szepeshazi, G. Halmos, and A. Nagy Preclinical Evaluation of Targeted Cytotoxic Luteinizing Hormone-Releasing Hormone Analogue AN-152 in Androgen-Sensitive and Insensitive Prostate Cancers Clin. Cancer Res., October 1, 2003; 9(12): 4505 - 4513. [Abstract] [Full Text] [PDF]
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 D. K. Lee and C. Chang Expression and Degradation of Androgen Receptor: Mechanism and Clinical Implication J. Clin. Endocrinol. Metab., September 1, 2003; 88(9): 4043 - 4054. [Abstract] [Full Text] [PDF]
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L. Yang, H.-K. Lin, S. Altuwaijri, S. Xie, L. Wang, and C. Chang APPL Suppresses Androgen Receptor Transactivation via Potentiating Akt Activity J. Biol. Chem., May 2, 2003; 278(19): 16820 - 16827. [Abstract] [Full Text] [PDF]
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N. J. Nesslinger, X.-B. Shi, and R. W. deVere White Androgen-independent Growth of LNCaP Prostate Cancer Cells Is Mediated by Gain-of-Function Mutant p53 Cancer Res., May 1, 2003; 63(9): 2228 - 2233. [Abstract] [Full Text] [PDF]
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G. E. Stoica, T. F. Franke, A. Wellstein, F. Czubayko, H.-J. List, R. Reiter, E. Morgan, M. B. Martin, and A. Stoica Estradiol Rapidly Activates Akt via the ErbB2 Signaling Pathway Mol. Endocrinol., May 1, 2003; 17(5): 818 - 830. [Abstract] [Full Text] [PDF]
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D. J. Lamb, E. Puxeddu, N. Malik, D. L. Stenoien, R. Nigam, G. Y. Saleh, M. Mancini, N. L. Weigel, and M. Marcelli Molecular Analysis of the Androgen Receptor in Ten Prostate Cancer Specimens Obtained Before and After Androgen Ablation J Androl, March 1, 2003; 24(2): 215 - 225. [Abstract] [Full Text] [PDF]
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R. M. Adam, J. Kim, J. Lin, A. Orsola, L. Zhuang, D. C. Rice, and M. R. Freeman* Heparin-Binding Epidermal Growth Factor-Like Growth Factor Stimulates Androgen-Independent Prostate Tumor Growth and Antagonizes Androgen Receptor Function Endocrinology, December 1, 2002; 143(12): 4599 - 4608. [Abstract] [Full Text] [PDF]
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I. K. Mellinghoff, C. Tran, and C. L. Sawyers Growth Inhibitory Effects of the Dual ErbB1/ErbB2 Tyrosine Kinase Inhibitor PKI-166 on Human Prostate Cancer Xenografts Cancer Res., September 15, 2002; 62(18): 5254 - 5259. [Abstract] [Full Text] [PDF]
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L. Xia, D. Robinson, A.-H. Ma, H.-C. Chen, F. Wu, Y. Qiu, and H.-J. Kung Identification of Human Male Germ Cell-associated Kinase, a Kinase Transcriptionally Activated by Androgen in Prostate Cancer Cells J. Biol. Chem., September 13, 2002; 277(38): 35422 - 35433. [Abstract] [Full Text] [PDF]
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M. Sharma, W. W. Chuang, and Z. Sun Phosphatidylinositol 3-Kinase/Akt Stimulates Androgen Pathway through GSK3beta Inhibition and Nuclear beta -Catenin Accumulation J. Biol. Chem., August 16, 2002; 277(34): 30935 - 30941. [Abstract] [Full Text] [PDF]
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D. Gioeli, S. B. Ficarro, J. J. Kwiek, D. Aaronson, M. Hancock, A. D. Catling, F. M. White, R. E. Christian, R. E. Settlage, J. Shabanowitz, et al. Androgen Receptor Phosphorylation. REGULATION AND IDENTIFICATION OF THE PHOSPHORYLATION SITES J. Biol. Chem., August 2, 2002; 277(32): 29304 - 29314. [Abstract] [Full Text] [PDF]
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 L. E. Lindberg, S. Hedjazifar, and D. Baeckstrom c-erbB2-induced Disruption of Matrix Adhesion and Morphogenesis Reveals a Novel Role for Protein Kinase B as a Negative Regulator of alpha 2beta 1 Integrin Function Mol. Biol. Cell, August 1, 2002; 13(8): 2894 - 2908. [Abstract] [Full Text] [PDF]
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D. J. Mulholland, H. Cheng, K. Reid, P. S. Rennie, and C. C. Nelson The Androgen Receptor Can Promote beta -Catenin Nuclear Translocation Independently of Adenomatous Polyposis Coli J. Biol. Chem., May 10, 2002; 277(20): 17933 - 17943. [Abstract] [Full Text] [PDF]
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L. Neckers Heat Shock Protein 90 Inhibition by 17-Allylamino-17- demethoxygeldanamycin: A Novel Therapeutic Approach for Treating Hormone-refractory Prostate Cancer : Commentary re: D. B. Solit et al., 17-Allylamino-17-demethoxygeldanamycin Induces the Degradation of Androgen Receptor and Her-2/neu and Inhibits the Growth of Prostate Cancer Xenografts. Clin. Cancer Res., 8: 986-993, 2002. Clin. Cancer Res., May 1, 2002; 8(5): 962 - 966. [Full Text] [PDF]
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D. B. Solit, F. F. Zheng, M. Drobnjak, P. N. Munster, B. Higgins, D. Verbel, G. Heller, W. Tong, C. Cordon-Cardo, D. B. Agus, et al. 17-Allylamino-17-demethoxygeldanamycin Induces the Degradation of Androgen Receptor and HER-2/neu and Inhibits the Growth of Prostate Cancer Xenografts Clin. Cancer Res., May 1, 2002; 8(5): 986 - 993. [Abstract] [Full Text] [PDF]
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L.-F. Lee, J. Guan, Y. Qiu, and H.-J. Kung Neuropeptide-Induced Androgen Independence in Prostate Cancer Cells: Roles of Nonreceptor Tyrosine Kinases Etk/Bmx, Src, and Focal Adhesion Kinase Mol. Cell. Biol., December 15, 2001; 21(24): 8385 - 8397. [Abstract] [Full Text] [PDF]
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H.-K. Lin, S. Yeh, H.-Y. Kang, and C. Chang Akt suppresses androgen-induced apoptosis by phosphorylating and inhibiting androgen receptor PNAS, June 7, 2001; (2001) 121173298. [Abstract] [Full Text] [PDF]
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M. Sumitomo, M. I. Milowsky, R. Shen, D. Navarro, J. Dai, T. Asano, M. Hayakawa, and D. M. Nanus Neutral Endopeptidase Inhibits Neuropeptide-mediated Transactivation of the Insulin-like Growth Factor Receptor-Akt Cell Survival Pathway Cancer Res., April 1, 2001; 61(8): 3294 - 3298. [Abstract] [Full Text]
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H.-K. Lin, S. Yeh, H.-Y. Kang, and C. Chang Akt suppresses androgen-induced apoptosis by phosphorylating and inhibiting androgen receptor PNAS, June 19, 2001; 98(13): 7200 - 7205. [Abstract] [Full Text] [PDF]
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