Epigenetic-induced repression of microRNA-205 is associated with MED1 activation and a poorer prognosis in localized prostate cancer

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Epigenetic-induced repression of microRNA-205 is associated with MED1 activation and a poorer prognosis in localized prostate cancer. / Hulf, T; Sibbritt, T; Wiklund, Erik Digman; Patterson, K; Song, J Z; Stirzaker, C; Qu, W; Nair, S; Horvath, L G; Armstrong, N J; Kench, J G; Sutherland, R L; Clark, S J.

I: Oncogene, Bind 32, Nr. 23, 06.06.2013, s. 2891-2899.

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avisTidsskriftartikelForskningpeer review

Harvard

Hulf, T, Sibbritt, T, Wiklund, ED, Patterson, K, Song, JZ, Stirzaker, C, Qu, W, Nair, S, Horvath, LG, Armstrong, NJ, Kench, JG, Sutherland, RL & Clark, SJ 2013, 'Epigenetic-induced repression of microRNA-205 is associated with MED1 activation and a poorer prognosis in localized prostate cancer', Oncogene, bind 32, nr. 23, s. 2891-2899. https://doi.org/10.1038/onc.2012.300

APA

Hulf, T., Sibbritt, T., Wiklund, E. D., Patterson, K., Song, J. Z., Stirzaker, C., Qu, W., Nair, S., Horvath, L. G., Armstrong, N. J., Kench, J. G., Sutherland, R. L., & Clark, S. J. (2013). Epigenetic-induced repression of microRNA-205 is associated with MED1 activation and a poorer prognosis in localized prostate cancer. Oncogene, 32(23), 2891-2899. https://doi.org/10.1038/onc.2012.300

CBE

Hulf T, Sibbritt T, Wiklund ED, Patterson K, Song JZ, Stirzaker C, Qu W, Nair S, Horvath LG, Armstrong NJ, Kench JG, Sutherland RL, Clark SJ. 2013. Epigenetic-induced repression of microRNA-205 is associated with MED1 activation and a poorer prognosis in localized prostate cancer. Oncogene. 32(23):2891-2899. https://doi.org/10.1038/onc.2012.300

MLA

Vancouver

Hulf T, Sibbritt T, Wiklund ED, Patterson K, Song JZ, Stirzaker C o.a. Epigenetic-induced repression of microRNA-205 is associated with MED1 activation and a poorer prognosis in localized prostate cancer. Oncogene. 2013 jun 6;32(23):2891-2899. https://doi.org/10.1038/onc.2012.300

Author

Hulf, T ; Sibbritt, T ; Wiklund, Erik Digman ; Patterson, K ; Song, J Z ; Stirzaker, C ; Qu, W ; Nair, S ; Horvath, L G ; Armstrong, N J ; Kench, J G ; Sutherland, R L ; Clark, S J. / Epigenetic-induced repression of microRNA-205 is associated with MED1 activation and a poorer prognosis in localized prostate cancer. I: Oncogene. 2013 ; Bind 32, Nr. 23. s. 2891-2899.

Bibtex

@article{4fd716e569e747599295eaa63c298e89,
title = "Epigenetic-induced repression of microRNA-205 is associated with MED1 activation and a poorer prognosis in localized prostate cancer",
abstract = "Deregulation of microRNA (miRNA) expression can have a critical role in carcinogenesis. Here we show in prostate cancer that miRNA-205 (miR-205) transcription is commonly repressed and the MIR-205 locus is hypermethylated. LOC642587, the MIR-205 host gene of unknown function, is also concordantly inactivated. We show that miR-205 targets mediator 1 (MED1, also called TRAP220 and PPARBP) for transcriptional silencing in normal prostate cells, leading to reduction in MED1 mRNA levels, and in total and active phospho-MED1 protein. Overexpression of miR-205 in prostate cancer cells negatively affects cell viability, consistent with a tumor suppressor function. We found that hypermethylation of the MIR-205 locus was strongly related with a decrease in miR-205 expression and an increase in MED1 expression in primary tumor samples (n=14), when compared with matched normal prostate (n=7). An expanded patient cohort (tumor n=149, matched normal n=30) also showed significant MIR-205 DNA methylation in tumors compared with normal, and MIR-205 hypermethylation is significantly associated with biochemical recurrence (hazard ratio=2.005, 95% confidence interval (1.109, 3.625), P=0.02), in patients with low preoperative prostate specific antigen. In summary, these results suggest that miR-205 is an epigenetically regulated tumor suppressor that targets MED1 and may provide a potential biomarker in prostate cancer management.",
keywords = "Adenocarcinoma, Aged, Base Sequence, Cell Line, Tumor, Cell Survival, DNA Methylation, Epigenesis, Genetic, Gene Expression Regulation, Neoplastic, Gene Silencing, Humans, Kaplan-Meier Estimate, Male, Mediator Complex Subunit 1, MicroRNAs, Middle Aged, Molecular Sequence Data, Phosphorylation, Prognosis, Promoter Regions, Genetic, Proportional Hazards Models, Prostatic Neoplasms, Protein Processing, Post-Translational",
author = "T Hulf and T Sibbritt and Wiklund, {Erik Digman} and K Patterson and Song, {J Z} and C Stirzaker and W Qu and S Nair and Horvath, {L G} and Armstrong, {N J} and Kench, {J G} and Sutherland, {R L} and Clark, {S J}",
year = "2013",
month = jun,
day = "6",
doi = "10.1038/onc.2012.300",
language = "English",
volume = "32",
pages = "2891--2899",
journal = "Oncogene",
issn = "0950-9232",
publisher = "Nature Publishing Group",
number = "23",

}

RIS

TY - JOUR

T1 - Epigenetic-induced repression of microRNA-205 is associated with MED1 activation and a poorer prognosis in localized prostate cancer

AU - Hulf, T

AU - Sibbritt, T

AU - Wiklund, Erik Digman

AU - Patterson, K

AU - Song, J Z

AU - Stirzaker, C

AU - Qu, W

AU - Nair, S

AU - Horvath, L G

AU - Armstrong, N J

AU - Kench, J G

AU - Sutherland, R L

AU - Clark, S J

PY - 2013/6/6

Y1 - 2013/6/6

N2 - Deregulation of microRNA (miRNA) expression can have a critical role in carcinogenesis. Here we show in prostate cancer that miRNA-205 (miR-205) transcription is commonly repressed and the MIR-205 locus is hypermethylated. LOC642587, the MIR-205 host gene of unknown function, is also concordantly inactivated. We show that miR-205 targets mediator 1 (MED1, also called TRAP220 and PPARBP) for transcriptional silencing in normal prostate cells, leading to reduction in MED1 mRNA levels, and in total and active phospho-MED1 protein. Overexpression of miR-205 in prostate cancer cells negatively affects cell viability, consistent with a tumor suppressor function. We found that hypermethylation of the MIR-205 locus was strongly related with a decrease in miR-205 expression and an increase in MED1 expression in primary tumor samples (n=14), when compared with matched normal prostate (n=7). An expanded patient cohort (tumor n=149, matched normal n=30) also showed significant MIR-205 DNA methylation in tumors compared with normal, and MIR-205 hypermethylation is significantly associated with biochemical recurrence (hazard ratio=2.005, 95% confidence interval (1.109, 3.625), P=0.02), in patients with low preoperative prostate specific antigen. In summary, these results suggest that miR-205 is an epigenetically regulated tumor suppressor that targets MED1 and may provide a potential biomarker in prostate cancer management.

AB - Deregulation of microRNA (miRNA) expression can have a critical role in carcinogenesis. Here we show in prostate cancer that miRNA-205 (miR-205) transcription is commonly repressed and the MIR-205 locus is hypermethylated. LOC642587, the MIR-205 host gene of unknown function, is also concordantly inactivated. We show that miR-205 targets mediator 1 (MED1, also called TRAP220 and PPARBP) for transcriptional silencing in normal prostate cells, leading to reduction in MED1 mRNA levels, and in total and active phospho-MED1 protein. Overexpression of miR-205 in prostate cancer cells negatively affects cell viability, consistent with a tumor suppressor function. We found that hypermethylation of the MIR-205 locus was strongly related with a decrease in miR-205 expression and an increase in MED1 expression in primary tumor samples (n=14), when compared with matched normal prostate (n=7). An expanded patient cohort (tumor n=149, matched normal n=30) also showed significant MIR-205 DNA methylation in tumors compared with normal, and MIR-205 hypermethylation is significantly associated with biochemical recurrence (hazard ratio=2.005, 95% confidence interval (1.109, 3.625), P=0.02), in patients with low preoperative prostate specific antigen. In summary, these results suggest that miR-205 is an epigenetically regulated tumor suppressor that targets MED1 and may provide a potential biomarker in prostate cancer management.

KW - Adenocarcinoma

KW - Aged

KW - Base Sequence

KW - Cell Line, Tumor

KW - Cell Survival

KW - DNA Methylation

KW - Epigenesis, Genetic

KW - Gene Expression Regulation, Neoplastic

KW - Gene Silencing

KW - Humans

KW - Kaplan-Meier Estimate

KW - Male

KW - Mediator Complex Subunit 1

KW - MicroRNAs

KW - Middle Aged

KW - Molecular Sequence Data

KW - Phosphorylation

KW - Prognosis

KW - Promoter Regions, Genetic

KW - Proportional Hazards Models

KW - Prostatic Neoplasms

KW - Protein Processing, Post-Translational

U2 - 10.1038/onc.2012.300

DO - 10.1038/onc.2012.300

M3 - Journal article

C2 - 22869146

VL - 32

SP - 2891

EP - 2899

JO - Oncogene

JF - Oncogene

SN - 0950-9232

IS - 23

ER -