miRNA and TMPRSS2-ERG do not mind their own business in prostate cancer cells

被引：13

作者：

Fayyaz, Sundas ^{[1
]}

Farooqi, Ammad Ahmad ^{[1
]}

机构：

[1] Rashid Latif Med Coll, Lab Translat Oncol & Personalized Med, Lahore, Pakistan

来源：

IMMUNOGENETICS | 2013年 / 65卷 / 05期

关键词：

TMPRSS2-ERG; Prostate cancer; miRNA; Signaling; AR; INDUCED CYTIDINE DEAMINASE; ANDROGEN RECEPTOR-ACTIVITY; MICRORNA EXPRESSION SIGNATURE; BETA-CATENIN CTNNB1; WNT/BETA-CATENIN; OXIDATIVE STRESS; CHROMOSOMAL REARRANGEMENTS; HEPATOCELLULAR-CARCINOMA; MESENCHYMAL TRANSITION; GENOMIC INSTABILITY;

D O I：

10.1007/s00251-012-0677-2

中图分类号：

Q3 [遗传学];

学科分类号：

071007 ; 090102 ;

摘要：

Oncogenic fusion proteins belong to an important class that disrupts gene expression networks in a cell. Astonishingly, fusion-positive prostate cancer cells enable the multi-gene regulatory capability of miRNAs to remodel the signal transduction landscape, enhancing or antagonizing the transmission of information to downstream effectors. Accumulating evidence substantiates the fact that miRNAs translate into dose-dependent responsiveness of cells to signaling regulators in transmembrane protease serine 2:ETS-related gene (TMPRSS2-ERG)-positive cells. Wide ranging signaling proteins are the targets for the degree of quantitative fluctuations imposed by miRNAs. miRNA signatures are aberrantly expressed in fusion-positive cancer cells, suggesting that they have a cumulative effect on tumor aggressiveness. It seems attractive to note that TMPRSS2:ERG fusion has a stronger effect as tumors positive for the oncogenic TMPRSS2:ERG have dysregulated oncomirs and tumor suppressor miRNA signature. It is undeniable that a comprehensive analysis of the prostate cancer microRNAome is necessary to uncover novel microRNAs and pathways associated with prostate cancer. Moreover, the identification and validation of miRNA signature in TMPRSS2-ERG-positive prostate cancer cells may help to identify novel molecular targets and pathways for personalized therapy.

引用

页码：315 / 332

页数：18

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