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Article: Oncofetal H19-derived miR-675 regulates tumor suppressor RB in human colorectal cancer

TitleOncofetal H19-derived miR-675 regulates tumor suppressor RB in human colorectal cancer
Authors
Issue Date2010
PublisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/
Citation
Carcinogenesis, 2010, v. 31 n. 3, p. 350-358 How to Cite?
AbstractH19 is an imprinted oncofetal non-coding RNA recently shown to be the precursor of miR-675. The pathophysiological roles of H19 and its mature product miR-675 to carcinogenesis have, however, not been defined. By quantitative reverse transcription-polymerase chain reaction, both H19 and miR-675 were found to be upregulated in human colon cancer cell lines and primary human colorectal cancer (CRC) tissues compared with adjacent noncancerous tissues. Subsequently, the tumor suppressor retinoblastoma (RB) was confirmed to be a direct target of miR-675 as the microRNA suppressed the activity of the luciferase reporter carrying the 3′-untranslated region of RB messenger RNA that contains the miR-675-binding site. Suppression of miR-675 by transfection with anti-miR-675 increased RB expression and at the same time, decreased cell growth and soft agar colony formation in human colon cancer cells. Reciprocally, enhanced miR-675 expression by transfection with miR-675 precursor decreased RB expression, increased tumor cell growth and soft agar colony formation. Moreover, the inverse relationship between the expressions of RB and H19/miR-675 was also revealed in human CRC tissues and colon cancer cell lines. Our findings demonstrate that H19-derived miR-675, through downregulation of its target RB, regulates the CRC development and thus may serve as a potential target for CRC therapy. © The Author 2009. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org.
Persistent Identifierhttp://hdl.handle.net/10722/92127
ISSN
2015 Impact Factor: 4.874
2015 SCImago Journal Rankings: 2.439
ISI Accession Number ID
Funding AgencyGrant Number
Hong Kong Research Grants CouncilCUHK4270/04M
Institute of Digestive Disease, Chinese University of Hong Kong
Funding Information:

Hong Kong Research Grants Council (Earmarked Grant CUHK4270/04M); Institute of Digestive Disease, Chinese University of Hong Kong.

References

 

DC FieldValueLanguage
dc.contributor.authorTsang, WPen_HK
dc.contributor.authorNg, EKOen_HK
dc.contributor.authorNg, SSMen_HK
dc.contributor.authorJin, Hen_HK
dc.contributor.authorYu, Jen_HK
dc.contributor.authorSung, JJYen_HK
dc.contributor.authorKwok, TTen_HK
dc.date.accessioned2010-09-17T10:36:53Z-
dc.date.available2010-09-17T10:36:53Z-
dc.date.issued2010en_HK
dc.identifier.citationCarcinogenesis, 2010, v. 31 n. 3, p. 350-358en_HK
dc.identifier.issn0143-3334en_HK
dc.identifier.urihttp://hdl.handle.net/10722/92127-
dc.description.abstractH19 is an imprinted oncofetal non-coding RNA recently shown to be the precursor of miR-675. The pathophysiological roles of H19 and its mature product miR-675 to carcinogenesis have, however, not been defined. By quantitative reverse transcription-polymerase chain reaction, both H19 and miR-675 were found to be upregulated in human colon cancer cell lines and primary human colorectal cancer (CRC) tissues compared with adjacent noncancerous tissues. Subsequently, the tumor suppressor retinoblastoma (RB) was confirmed to be a direct target of miR-675 as the microRNA suppressed the activity of the luciferase reporter carrying the 3′-untranslated region of RB messenger RNA that contains the miR-675-binding site. Suppression of miR-675 by transfection with anti-miR-675 increased RB expression and at the same time, decreased cell growth and soft agar colony formation in human colon cancer cells. Reciprocally, enhanced miR-675 expression by transfection with miR-675 precursor decreased RB expression, increased tumor cell growth and soft agar colony formation. Moreover, the inverse relationship between the expressions of RB and H19/miR-675 was also revealed in human CRC tissues and colon cancer cell lines. Our findings demonstrate that H19-derived miR-675, through downregulation of its target RB, regulates the CRC development and thus may serve as a potential target for CRC therapy. © The Author 2009. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org.en_HK
dc.languageengen_HK
dc.publisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/en_HK
dc.relation.ispartofCarcinogenesisen_HK
dc.subject.meshAdenocarcinoma - genetics - pathology-
dc.subject.meshCell Transformation, Neoplastic - genetics-
dc.subject.meshColorectal Neoplasms - genetics - pathology-
dc.subject.meshMicroRNAs - genetics - physiology-
dc.subject.meshNeoplasm Proteins - physiology-
dc.titleOncofetal H19-derived miR-675 regulates tumor suppressor RB in human colorectal canceren_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0143-3334&volume=31&issue=3&spage=350&epage=358&date=2010&atitle=Oncofetal+H19-derived+miR-675+regulates+tumor+suppressor+RB+in+human+colorectal+cancer-
dc.identifier.emailNg, EKO: ngko@hku.hken_HK
dc.identifier.authorityNg, EKO=rp01364en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1093/carcin/bgp181en_HK
dc.identifier.pmid19926638en_HK
dc.identifier.scopuseid_2-s2.0-77950881915en_HK
dc.identifier.hkuros172814-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77950881915&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume31en_HK
dc.identifier.issue3en_HK
dc.identifier.spage350en_HK
dc.identifier.epage358en_HK
dc.identifier.eissn1460-2180-
dc.identifier.isiWOS:000275245200004-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridTsang, WP=7201558605en_HK
dc.identifier.scopusauthoridNg, EKO=21135553700en_HK
dc.identifier.scopusauthoridNg, SSM=26021413400en_HK
dc.identifier.scopusauthoridJin, H=24577511700en_HK
dc.identifier.scopusauthoridYu, J=35351306800en_HK
dc.identifier.scopusauthoridSung, JJY=35405352400en_HK
dc.identifier.scopusauthoridKwok, TT=35196382300en_HK

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