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Review
. 2018 Aug;10(4):1205-1213.
doi: 10.1007/s12551-017-0379-y. Epub 2017 Dec 8.

Long non-coding RNA expression in bladder cancer

Mohammad Taheri  1   2 , Mir Davood Omrani  1   2 , Soudeh Ghafouri-Fard  3
Affiliations
Review

Long non-coding RNA expression in bladder cancer

Mohammad Taheri et al. Biophys Rev. 2018 Aug.

Abstract

The advent of novel high-throughput sequencing methods has facilitated identification of non-coding RNAs with fundamental roles in cellular biological and pathological conditions. A group of these consisting of at least 200 nucleotides are called long non-coding RNAs (lncRNAs). Their participation in the pathogenesis of cancer has been highlighted in recent years. Bladder cancer, one of the most prevalent cancers worldwide, exhibits altered expression levels of several lncRNAs. Several in vitro and in vivo studies have assessed the effects of silencing RNAs on cancer cell phenotypes and in vivo tumor growth. For instance, in vitro studies have shown that nuclear paraspeckle assembly transcript 1 (NEAT1), promoter of CDKN1A antisense DNA damage-activated RNA(PANDAR) and metastasis-associated lung adenocarcinoma transcript 1(MALAT1) have oncogenic effects while Maternally expressed 3 (MEG3) and BRAF activated non-coding RNA (BANCR) are tumor suppressors. Analysis of these data will help to identify a panel of lncRNAs that can be potentially used for both early detection and prognosis in bladder cancer patients. Here, we review the roles of several lncRNAs in the oncogenesis, tumor suppression, early detection, and prognosis of bladder cancer.

Keywords: Bladder cancer; Cancer prognosis; Oncogenesis; Tumor suppression; lncRNA.

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Conflict of interest statement

Mohammad Taheri declares that he has no conflicts of interest. Mir Davood Omrani declares that he has no conflicts of interest. Soudeh Ghafouri-Fard declares that she has no conflicts of interest.

This article does not contain any studies with human participants or animals performed by any of the authors.

Figures

Fig. 1
Fig. 1
TUG1 participation in bladder cancer: TUG1 interacts with PRC2 and EZH2 and promotes methylation of several proteins with inhibitory effects in cell cycle pregreesion
Fig. 2
Fig. 2
H19 participation in bladder cancer: H19 overexpression leads to upregulation of ID2 and down-regulation of E-cadherin. The former effect results in suppression of Rbm p16 and p21. The latter leads to metastasis
Fig. 3
Fig. 3
PVT1 participation in bladder cance. a PVT1 overexpression inhibits MYC phosphorylation and its degaradtion in proteasomes. b PVT1 locus acts as a molecular switch for determination of cell fate
Fig. 4
Fig. 4
ANRIL participation in bladder cancer: ANRIL overexpression lead to up-regulation of anti-apoptotic genes while down-regulation of pro-apoptotic genes
See this image and copyright information in PMC

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