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Series GSE123517 Query DataSets for GSE123517
Status Public on Mar 01, 2019
Title Effects of OCT1 knockdown in castration-resistant prostate cancer cells
Organism Homo sapiens
Experiment type Expression profiling by array
Summary Prostate cancer is the most common cancer in men and AR downstream signalings promote prostate cancer cell proliferation. Although initially hormone-deprovation therapy is effective to inhibit cancer progression, most of cancers relapse as castration-resistant prostate cancer (CRPC). Therefore, we examined the effect of AR interacting partner OCT1 in CRPC cells.
In order to investigate the OCT1 function in CRPC cells, we performed gene expression in AR-positive CRPC cell line, 22Rv1, after siOCT1 treatment. We also treated cells with vehicle or dihydrotestosterone (DHT) to analyzed the effects of OCT1 on AR function.
 
Overall design Observation of androgen dependent gene expression changes in CRPC after treatmet with siRNAs targeting OCT1 using microarray.
 
Contributor(s) Takayama K, Inoue S
Citation(s) 31454442
Submission date Dec 07, 2018
Last update date Nov 12, 2019
Contact name Ken-ichi Takayama
Organization name Tokyo Metropolitan Institute of Gerontology
Street address Sakaecho
City Itabashi-ku
ZIP/Postal code 173-0015
Country Japan
 
Platforms (1)
GPL23159 [Clariom_S_Human] Affymetrix Clariom S Assay, Human (Includes Pico Assay)
Samples (4)
GSM3506027 22Rv1_siControl_Veh
GSM3506028 22Rv1_siControl_DHT
GSM3506029 22Rv1_siOCT1_Veh
Relations
BioProject PRJNA508978

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE123517_RAW.tar 5.0 Mb (http)(custom) TAR (of CEL, CHP)
Processed data included within Sample table
Processed data provided as supplementary file

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