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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
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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.
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Overall design |
Observation of androgen dependent gene expression changes in CRPC after treatmet with siRNAs targeting OCT1 using microarray.
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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
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Street address |
Sakaecho
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City |
Itabashi-ku |
ZIP/Postal code |
173-0015 |
Country |
Japan |
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Platforms (1) |
GPL23159 |
[Clariom_S_Human] Affymetrix Clariom S Assay, Human (Includes Pico Assay) |
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Samples (4)
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Relations |
BioProject |
PRJNA508978 |