RGD Reference Report - Deregulated expression of selected histone methylases and demethylases in prostate carcinoma. - Rat Genome Database

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Deregulated expression of selected histone methylases and demethylases in prostate carcinoma.

Authors: Vieira, FQ  Costa-Pinheiro, P  Ramalho-Carvalho, J  Pereira, A  Menezes, FD  Antunes, L  Carneiro, I  Oliveira, J  Henrique, R  Jeronimo, C 
Citation: Vieira FQ, etal., Endocr Relat Cancer. 2013 Dec 16;21(1):51-61. doi: 10.1530/ERC-13-0375. Print 2014 Feb.
RGD ID: 9587761
Pubmed: PMID:24200674   (View Abstract at PubMed)
DOI: DOI:10.1530/ERC-13-0375   (Journal Full-text)

Prostate cancer (PCa), a leading cause of cancer-related morbidity and mortality, arises through the acquisition of genetic and epigenetic alterations. Deregulation of histone methyltransferases (HMTs) or demethylases (HDMs) has been associated with PCa development and progression. However, the precise influence of altered HMTs or HDMs expression and respective histone marks in PCa onset and progression remains largely unknown. To clarify the role of HMTs and HDMs in prostate carcinogenesis, expression levels of 37 HMTs and 20 HDMs were assessed in normal prostate and PCa tissue samples by RT-qPCR. SMYD3, SUV39H2, PRMT6, KDM5A, and KDM6A were upregulated, whereas KMT2A-E (MLL1-5) and KDM4B were downregulated in PCa, compared with normal prostate tissues. Remarkably, PRMT6 was the histone modifier that best discriminated normal from tumorous tissue samples. Interestingly, EZH2 and SMYD3 expression levels significantly correlated with less differentiated and more aggressive tumors. Remarkably, SMYD3 expression levels were of independent prognostic value for the prediction of disease-specific survival of PCa patients with clinically localized disease submitted to radical prostatectomy. We concluded that expression profiling of HMTs and HDMs, especially SMYD3, might be of clinical usefulness for the assessment of PCa patients and assist in pre-therapeutic decision-making.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
prostate cancer  IEP 9587761; 9587761; 9587761; 9587761; 9587761; 9587761; 9587761mRNA:decreased expression:prostate gland (human)RGD 
prostate cancer  ISOKDM5A (Homo sapiens)9587761; 9587761mRNA:decreased expression:prostate gland (human)RGD 
prostate cancer  ISOKDM6A (Homo sapiens)9587761mRNA:decreased expression:prostate gland (human)RGD 
prostate cancer  ISOKMT2A (Homo sapiens)9587761; 9587761mRNA:decreased expression:prostate gland (human)RGD 
prostate cancer  ISOKMT2B (Homo sapiens)9587761; 9587761mRNA:decreased expression:prostate gland (human)RGD 
prostate cancer  ISOKMT2C (Homo sapiens)9587761; 9587761mRNA:decreased expression:prostate gland (human)RGD 
prostate cancer  ISOKMT2D (Homo sapiens)9587761; 9587761mRNA:decreased expression:prostate gland (human)RGD 
prostate cancer  ISOKMT2E (Homo sapiens)9587761; 9587761mRNA:decreased expression:prostate gland (human)RGD 
Prostatic Neoplasms  ISOKDM6A (Homo sapiens)9587761mRNA:decreased expression:prostate gland (human)RGD 

Objects Annotated

Genes (Rattus norvegicus)
Kdm5a  (lysine demethylase 5A)
Kmt2a  (lysine methyltransferase 2A)
Kmt2b  (lysine methyltransferase 2B)
Kmt2c  (lysine methyltransferase 2C)
Kmt2d  (lysine methyltransferase 2D)
Kmt2e  (lysine methyltransferase 2E)
Uty  (ubiquitously transcribed tetratricopeptide repeat containing, Y-linked)

Genes (Mus musculus)
Kdm5a  (lysine demethylase 5A)
Kdm6a  (lysine (K)-specific demethylase 6A)
Kmt2a  (lysine (K)-specific methyltransferase 2A)
Kmt2b  (lysine (K)-specific methyltransferase 2B)
Kmt2c  (lysine (K)-specific methyltransferase 2C)
Kmt2d  (lysine (K)-specific methyltransferase 2D)
Kmt2e  (lysine (K)-specific methyltransferase 2E)

Genes (Homo sapiens)
KDM5A  (lysine demethylase 5A)
KDM6A  (lysine demethylase 6A)
KMT2A  (lysine methyltransferase 2A)
KMT2B  (lysine methyltransferase 2B)
KMT2C  (lysine methyltransferase 2C)
KMT2D  (lysine methyltransferase 2D)
KMT2E  (lysine methyltransferase 2E (inactive))


Additional Information