The role of epigenetics and long noncoding RNA MIAT in neuroendocrine prostate cancer

被引：95

作者：

Crea, Francesco ^{[1
,2
]}

Venalainen, Erik ^{[1
]}

Ci, Xinpei ^{[1
,3
]}

Cheng, Hongwei ^{[1
]}

Pikor, Larissa ^{[4
]}

Parolia, Abhijit ^{[1
]}

Xue, Hui ^{[1
]}

Saidy, Nur Ridzwan Nur ^{[1
]}

Lin, Dong ^{[1
,3
]}

Lam, Wan ^{[4
]}

Collins, Colin ^{[3
]}

Wang, Yuzhuo ^{[1
,3
]}

机构：

[1] BC Canc Agcy Canc Res Ctr, Expt Therapeut, Vancouver, BC, Canada

[2] Open Univ, Dept Life Hlth & Chem Sci, Milton Keynes MK7 6AA, Bucks, England

[3] Univ British Columbia, Vancouver Prostate Ctr, Dept Urol Sci, Vancouver, BC, Canada

[4] BC Canc Agcy Canc Res Ctr, Genet Unit, Integrat Oncol, Vancouver, BC, Canada

来源：

EPIGENOMICS | 2016年 / 8卷 / 05期

基金：

加拿大健康研究院;

关键词：

epigenetic/noncoding interactome; long noncoding RNAs; MIAT; neuroendocrine prostate cancer; Polycomb; transdifferentiation; TRANSCRIPTIONAL NOISE; MOLECULAR-GENETICS; TUMOR PROGRESSION; CELL; MICRORNA; DIFFERENTIATION; EZH2; ADENOCARCINOMA; SURVIVAL; IDENTIFICATION;

D O I：

10.2217/epi.16.6

中图分类号：

Q3 [遗传学];

学科分类号：

071007 ; 090102 ;

摘要：

Neuroendocrine prostate cancer (NEPC) is the most lethal prostatic neoplasm. NEPC is thought to originate from the transdifferentiation of AR-positive adenocarcinoma cells. We have previously shown that an epigenetic/noncoding interactome (ENI) orchestrates cancer cells' plasticity, thereby allowing the emergence of metastatic, drug-resistant neoplasms. The primary objective of this manuscript is to discuss evidence indicating that some components of the ENI (Polycomb genes, miRNAs) play a key role in NEPC initiation and progression. Long noncoding RNAs represent vast and largely unexplored component of the ENI. Their role in NEPC has not been investigated. We show preliminary evidence indicating that a lncRNA (MIAT) is selectively upregulated in NEPCs and might interact with Polycomb genes. Our results indicate that long noncoding RNAs can be exploited as new biomarkers and therapeutic targets for NEPC.

引用

页码：721 / 731

页数：11

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