TY - JOUR
T1 - MicroRNA let-7c suppresses androgen receptor expression and activity via regulation of myc expression in prostate cancer cells
AU - Nadiminty, N.
AU - Tummala, R.
AU - Lou, W.
AU - Zhu, Y.
AU - Zhang, J.
AU - Chen, X.
AU - DeVere White, R.W.
AU - Kung, H.-J.
AU - Evans, C.P.
AU - Gao, A.C.
N1 - 引用次數:103
Export Date: 5 March 2018
CODEN: JBCHA
通訊地址: Nadiminty, N.; Department of Urology, University of California Davis Medical Center, Research III, 4645 2nd Ave, Sacramento, CA 95817, United States; 電子郵件: [email protected]
化學物質/CAS: LIN-28 protein, human; MYC protein, human; MicroRNAs; Proto-Oncogene Proteins c-myc; RNA, Neoplasm; RNA-Binding Proteins; Receptors, Androgen; mirnlet7 microRNA, human
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PY - 2012/1
Y1 - 2012/1
N2 - Castration-resistant prostate cancer continues to rely on androgen receptor (AR) expression. AR plays a central role in the development of prostate cancer and progression to castration resistance during and after androgen deprivation therapy. Here, we identified miR-let-7c as a key regulator of expression of AR. miR-let-7c suppresses AR expression and activity in human prostate cancer cells by targeting its transcription via c-Myc. Suppression of AR by let-7c leads to decreased cell proliferation of human prostate cancer cells. Down-regulation of Let-7c in prostate cancer specimens is inversely correlated with AR expression, whereas the expression of Lin28 (a repressor of let-7) is correlated positively with AR expression. Our study demonstrates that the miRNA let-7c plays an important role in the regulation of androgen signaling in prostate cancer by down-regulating AR expression. These results suggest that reconstitution of miR-let-7c may aid in targeting enhanced and hypersensitive AR in advanced prostate cancer. © 2012 by The American Society for Biochemistry and Molecular Biology, Inc.
AB - Castration-resistant prostate cancer continues to rely on androgen receptor (AR) expression. AR plays a central role in the development of prostate cancer and progression to castration resistance during and after androgen deprivation therapy. Here, we identified miR-let-7c as a key regulator of expression of AR. miR-let-7c suppresses AR expression and activity in human prostate cancer cells by targeting its transcription via c-Myc. Suppression of AR by let-7c leads to decreased cell proliferation of human prostate cancer cells. Down-regulation of Let-7c in prostate cancer specimens is inversely correlated with AR expression, whereas the expression of Lin28 (a repressor of let-7) is correlated positively with AR expression. Our study demonstrates that the miRNA let-7c plays an important role in the regulation of androgen signaling in prostate cancer by down-regulating AR expression. These results suggest that reconstitution of miR-let-7c may aid in targeting enhanced and hypersensitive AR in advanced prostate cancer. © 2012 by The American Society for Biochemistry and Molecular Biology, Inc.
KW - Androgen deprivation therapy
KW - Androgen receptors
KW - Down-regulation
KW - Human prostate cancer cells
KW - Key regulators
KW - MicroRNAs
KW - Prostate cancer cells
KW - Prostate cancers
KW - Cell proliferation
KW - Cells
KW - Diseases
KW - androgen receptor
KW - microRNA
KW - microRNA let 7c
KW - Myc protein
KW - unclassified drug
KW - article
KW - binding site
KW - cancer cell culture
KW - cell proliferation
KW - cell survival
KW - chromatin immunoprecipitation
KW - controlled study
KW - down regulation
KW - enzyme reconstitution
KW - gene expression regulation
KW - gene overexpression
KW - genetic transcription
KW - human
KW - human cell
KW - plasmid
KW - priority journal
KW - promoter region
KW - prostate cancer
KW - protein analysis
KW - protein binding
KW - signal transduction
KW - upregulation
KW - Cell Line, Tumor
KW - Cell Proliferation
KW - Gene Expression Regulation, Neoplastic
KW - Humans
KW - Male
KW - Prostatic Neoplasms
KW - Proto-Oncogene Proteins c-myc
KW - Receptors, Androgen
KW - RNA, Neoplasm
KW - RNA-Binding Proteins
KW - Signal Transduction
U2 - 10.1074/jbc.M111.278705
DO - 10.1074/jbc.M111.278705
M3 - Article
SN - 0021-9258
VL - 287
SP - 1527
EP - 1537
JO - Journal of Biological Chemistry
JF - Journal of Biological Chemistry
IS - 2
ER -
