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<biogps><data><item key="platform">8</item><item key="owner">ArrayExpress Uploader</item><item key="pop_total">0</item><item key="species">mouse</item><item key="factors"><item><item key="GSM718745"><item key="TIME">control</item></item></item><item><item key="GSM718745"><item key="TIME">control</item></item></item><item><item key="GSM718747"><item key="TIME">0 h</item></item></item><item><item key="GSM718747"><item key="TIME">0 h</item></item></item><item><item key="GSM718749"><item key="TIME">24 h</item></item></item><item><item key="GSM718749"><item key="TIME">24 h</item></item></item><item><item key="GSM71875"><item key="TIME">48 h</item></item></item><item><item key="GSM71875"><item key="TIME">48 h</item></item></item></item><item key="id">8550</item><item key="ownerprofile_id">arrayexpress_sid</item><item key="source">http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-29010</item><item key="summary_wrapped">Alteration of the PTEN/PI3K pathway is associated with late stage and castrate resistant prostate cancer (CRPC).  However, how PTEN loss...</item><item key="owner_profile">/profile/8773/arrayexpressuploader</item><item key="factor_count">1</item><item key="sample_count">8</item><item key="tags"><item>androgen</item><item>cancer</item><item>point</item><item>prostate</item><item>prostate cancer</item><item>viral infection</item></item><item key="lastmodified">Dec.12, 2014</item><item key="is_default">False</item><item key="geo_gds_id"/><item key="slug">cell-autonomous-role-of-pten-in-regulating-castrat</item><item key="geo_id_plat">E-GEOD-29010_A-AFFY-36</item><item key="name">Cell autonomous role of PTEN in regulating castration-resistant prostate cancer growth</item><item key="created">Nov.24, 2014</item><item key="summary">Alteration of the PTEN/PI3K pathway is associated with late stage and castrate resistant prostate cancer (CRPC).  However, how PTEN loss involves in CRPC development is not clear.  Here we show that castration-resistant growth is an intrinsic property of Pten-null prostate cancer (CaP) cells, independent of cancer development stage.PTEN loss suppresses androgen-responsive gene expressions by modulating androgen receptor (AR) transcription factor activity. Conditional deletion of AR in the epithelium promotes the proliferation of Pten-null cancer cells, at least in part, by down-regulating androgen-responsive gene FKBP5 and preventing PHLPP-mediated AKT inhibition. Our findings identify PI3K and AR pathway crosstalk as a mechanism of CRPC development, with potentially important implications for CaP etiology and therapy Mouse embryonic fibroblasts (MEFs) carrying a tet-inducible Pten transgene were generated by retro viral infection and antibiotic selection.  Cells were treated with 2 ug/ml doxycycline for 24 or 48 hours in tet-free FBS (5%)/MEF media (n=2).  Reference samples were either cells before treatment (n=2).  After each time point cells were washed twice with PBS and RNA trizol extracted.  WT samples (n =2) were also included as a control.</item><item key="geo_gse_id">E-GEOD-29010</item><item key="sample_source">http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-29010/samples/</item></data></biogps>
