Abstract | BACKGROUND: MATERIALS & METHODS: RAI16 expression was detected in prostate cancer cells with or without the AR agonist R1881 treatment by quantitative RT-PCR and Western blot. Direct AR binding to the RAI16 promoter was tested using AR chromatin immunoprecipitation (ChIP) and luciferase assay. Cell viability and colony formation assays in response to R1881 were analyzed in cells with RAI16 knockdown by specific siRNA. RESULTS: The expression of RAI16 was high in LNCaP(AI), LNCaP(AD), C4-2 expressing AR, but low in Du145 and Pc-3 cells without AR expressing. In addition, the expression of RAI16 could be induced by 10 nM R1881 treatment LNCaP(AD) and C4-2 cells, but inhibited by AR specific siRNA treatment. Furthermore, AR binds directly to ARE3 (-2003~-1982bp) of RAI16 promoter region by ChIP and luciferase assay. RAI16 knockdown inhibited the enhancement of cell viability and colony formation of AR stimulation. CONCLUSIONS: We demonstrate for the first time that RAI16 is a direct target gene of AR. RAI16 may involved in cell growth of prostate cancer cells in response to AR signaling.
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Authors | Cui-Ling Ding, Chun-Lin Qian, Zhong-Tian Qi, Wen Wang |
Journal | Molecular and cellular endocrinology
(Mol Cell Endocrinol)
Vol. 506
Pg. 110745
(04 15 2020)
ISSN: 1872-8057 [Electronic] Ireland |
PMID | 32014455
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 2020 Elsevier B.V. All rights reserved. |
Chemical References |
- AR protein, human
- Androgens
- FAM160B2 protein, human
- Proteins
- Receptors, Androgen
- Metribolone
|
Topics |
- Adenocarcinoma
(genetics, pathology)
- Androgens
(pharmacology)
- Cell Line, Tumor
- Gene Expression Regulation, Neoplastic
(drug effects)
- Humans
- Male
- Metribolone
(pharmacology)
- PC-3 Cells
- Promoter Regions, Genetic
(drug effects)
- Prostatic Neoplasms
(genetics, pathology)
- Protein Binding
(drug effects)
- Proteins
(genetics, physiology)
- Receptors, Androgen
(metabolism, physiology)
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