Document Detail


The role of microRNA-221 and microRNA-222 in androgen-independent prostate cancer cell lines.
MedLine Citation:
PMID:  19351832     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Androgen-dependent prostate cancer typically progresses to castration-resistant prostate cancer (CRPC) after the androgen deprivation therapy. MicroRNAs (miR) are noncoding small RNAs (19-25nt) that play an important role in the regulation of gene expression. Recent studies have shown that miR expression patterns are significantly different in normal and neoplastic prostate epithelial cells. However, the importance of miRs in the development of CRPC has not yet been explored. By performing genome-wide expression profiling of miRs, we found that expression levels of several miRs, in particular miR-221 and miR-222, were significantly increased in CRPC cells (the LNCaP-derived cell line LNCaP-Abl), compared with those in the androgen-dependent prostate cancer cell line (LNCaP). Overexpression of miR-221 or miR-222 in LNCaP or another androgen-dependent cell line, LAPC-4, significantly reduced the level of the dihydrotestosterone (DHT) induced up-regulation of prostate-specific antigen (PSA) expression and increased androgen-independent growth of LNCaP cells. Knocking down the expression level of miR-221 and miR-222 with antagonist miRs in the LNCaP-Abl cell line restored the response to the DHT induction of PSA transcription and also increased the growth response of the LNCaP-Abl cells to the androgen treatment. Changing the expression level of p27/kip1, a known target of miR-221 and miR-222, alone in LNCaP cells affected the DHT-independent cell growth but did not significantly influence the response of PSA transcription to the DHT treatment. In conclusion, our data suggest the involvement of miR-221 and miR-222 in the development or maintenance of the CRPC phenotype.
Authors:
Tong Sun; Qianben Wang; Steven Balk; Myles Brown; Gwo-Shu Mary Lee; Philip Kantoff
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2009-04-07
Journal Detail:
Title:  Cancer research     Volume:  69     ISSN:  1538-7445     ISO Abbreviation:  Cancer Res.     Publication Date:  2009 Apr 
Date Detail:
Created Date:  2009-04-16     Completed Date:  2009-06-19     Revised Date:  2013-06-02    
Medline Journal Info:
Nlm Unique ID:  2984705R     Medline TA:  Cancer Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  3356-63     Citation Subset:  IM    
Affiliation:
Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA 02115, USA.
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MeSH Terms
Descriptor/Qualifier:
Androgens / metabolism
Cell Growth Processes / drug effects,  genetics
Cell Line, Tumor
Dihydrotestosterone / pharmacology
Gene Expression / drug effects
Humans
Male
MicroRNAs / biosynthesis*,  genetics
Neoplasms, Hormone-Dependent / genetics
Prostatic Neoplasms / genetics*
Receptors, Androgen / genetics,  metabolism
Transcription, Genetic / drug effects
Transfection
Grant Support
ID/Acronym/Agency:
2 P50 CA090381-06/CA/NCI NIH HHS; P50 CA090381/CA/NCI NIH HHS; P50 CA090381-06/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Androgens; 0/MIRN221 microRNA, human; 0/MIRN222 microRNA, human; 0/MicroRNAs; 0/Receptors, Androgen; 521-18-6/Dihydrotestosterone
Comments/Corrections

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