File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Adenosine-to-inosine RNA editing mediated by ADARs in esophageal squamous cell carcinoma

TitleAdenosine-to-inosine RNA editing mediated by ADARs in esophageal squamous cell carcinoma
Authors
Issue Date2014
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/
Citation
Cancer Research, 2014, v. 74 n. 3, p. 840-851 How to Cite?
AbstractEsophageal squamous cell carcinoma (ESCC), the major histologic form of esophageal cancer, is a heterogeneous tumor displaying a complex variety of genetic and epigenetic changes. Aberrant RNA editing of adenosine-to-inosine (A-to-I), as it is catalyzed by adenosine deaminases acting on RNA (ADAR), represents a common posttranscriptional modification in certain human diseases. In this study, we investigated the status and role of ADARs and altered A-to-I RNA editing in ESCC tumorigenesis. Among the three ADAR enzymes expressed in human cells, only ADAR1 was overexpressed in primary ESCC tumors. ADAR1 overexpression was due to gene amplification. Patients with ESCC with tumoral overexpression of ADAR1 displayed a poor prognosis. In vitro and in vivo functional assays established that ADAR1 functions as an oncogene during ESCC progression. Differential expression of ADAR1 resulted in altered gene-specific editing activities, as reflected by hyperediting of FLNB and AZIN1 messages in primary ESCC. Notably, the edited form of AZIN1 conferred a gain-of-function phenotype associated with aggressive tumor behavior. Our findings reveal that altered gene-specific A-to-I editing events mediated by ADAR1 drive the development of ESCC, with potential implications in diagnosis, prognosis, and treatment of this disease.
Persistent Identifierhttp://hdl.handle.net/10722/198471
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorQin, YR-
dc.contributor.authorQiao, JJ-
dc.contributor.authorChan, THM-
dc.contributor.authorZhu, YH-
dc.contributor.authorLi, FF-
dc.contributor.authorLiu, H-
dc.contributor.authorFei, J-
dc.contributor.authorLi, Y-
dc.contributor.authorGuan, X-
dc.contributor.authorChen, L-
dc.date.accessioned2014-07-07T07:08:12Z-
dc.date.available2014-07-07T07:08:12Z-
dc.date.issued2014-
dc.identifier.citationCancer Research, 2014, v. 74 n. 3, p. 840-851-
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/198471-
dc.description.abstractEsophageal squamous cell carcinoma (ESCC), the major histologic form of esophageal cancer, is a heterogeneous tumor displaying a complex variety of genetic and epigenetic changes. Aberrant RNA editing of adenosine-to-inosine (A-to-I), as it is catalyzed by adenosine deaminases acting on RNA (ADAR), represents a common posttranscriptional modification in certain human diseases. In this study, we investigated the status and role of ADARs and altered A-to-I RNA editing in ESCC tumorigenesis. Among the three ADAR enzymes expressed in human cells, only ADAR1 was overexpressed in primary ESCC tumors. ADAR1 overexpression was due to gene amplification. Patients with ESCC with tumoral overexpression of ADAR1 displayed a poor prognosis. In vitro and in vivo functional assays established that ADAR1 functions as an oncogene during ESCC progression. Differential expression of ADAR1 resulted in altered gene-specific editing activities, as reflected by hyperediting of FLNB and AZIN1 messages in primary ESCC. Notably, the edited form of AZIN1 conferred a gain-of-function phenotype associated with aggressive tumor behavior. Our findings reveal that altered gene-specific A-to-I editing events mediated by ADAR1 drive the development of ESCC, with potential implications in diagnosis, prognosis, and treatment of this disease.-
dc.languageeng-
dc.publisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/-
dc.relation.ispartofCancer Research-
dc.subject.meshAdenosine Deaminase - genetics - metabolism-
dc.subject.meshCarcinoma, Squamous Cell - genetics - metabolism - mortality-
dc.subject.meshEsophageal Neoplasms - genetics - metabolism - mortality-
dc.subject.meshInosine-
dc.subject.meshRNA Editing-
dc.titleAdenosine-to-inosine RNA editing mediated by ADARs in esophageal squamous cell carcinoma-
dc.typeArticle-
dc.identifier.emailChan, THM: chantim@hkucc.hku.hk-
dc.identifier.emailLi, Y: vikkiyan@hku.hk-
dc.identifier.emailGuan, X: xyguan@hkucc.hku.hk-
dc.identifier.emailChen, L: pollyllc@hku.hk-
dc.identifier.authorityGuan, X=rp00454-
dc.identifier.doi10.1158/0008-5472.CAN-13-2545-
dc.identifier.pmid24302582-
dc.identifier.scopuseid_2-s2.0-84893833808-
dc.identifier.hkuros229764-
dc.identifier.volume74-
dc.identifier.issue3-
dc.identifier.spage840-
dc.identifier.epage851-
dc.identifier.isiWOS:000331073900021-
dc.publisher.placeUnited States-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats