File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Article: A contrasting function for miR-137 in embryonic mammogenesis and adult breast carcinogenesis

TitleA contrasting function for miR-137 in embryonic mammogenesis and adult breast carcinogenesis
Authors
KeywordsBreast cancer
Mammary gland development
MiR-137
Tachykinin-1
Tumour suppressor
Issue Date2015
PublisherImpact Journals LLC. The Journal's web site is located at http://www.impactjournals.com/oncotarget/index.html
Citation
Oncotarget, 2015, v. 6 n. 26, p. 22048-22059 How to Cite?
AbstractMicroRNAs are differentially expressed in breast cancer cells and have been implicated in cancer formation, tumour invasion and metastasis. We investigated the miRNA expression profiles in the developing mammary gland. MiR-137 was expressed prominently in the developing mammary gland. When the miR-137 was over-expressed in the embryo, the mammary epithelium became thickened. Moreover, genes associated with mammary gland formation such as Tbx3 and Lef1 were not expressed. This suggests that miR-137 induces gland formation and invasion. When miR-137 was over-expressed in MDA-MB-231 cells, their ability to form tumours in adult mice was significantly reduced. These data support miR-137 decides epithelial cell behavior in the human breast cancer. It also suggests that miR-137 is a potential therapeutic target for amelioration of breast cancer progression.
Persistent Identifierhttp://hdl.handle.net/10722/215048
ISSN
2016 Impact Factor: 5.168
2020 SCImago Journal Rankings: 1.373
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLee, JM-
dc.contributor.authorCho, KW-
dc.contributor.authorKim, EJ-
dc.contributor.authorTang, Q-
dc.contributor.authorKim, KS-
dc.contributor.authorTickle, C-
dc.contributor.authorJung, HS-
dc.date.accessioned2015-08-21T12:21:01Z-
dc.date.available2015-08-21T12:21:01Z-
dc.date.issued2015-
dc.identifier.citationOncotarget, 2015, v. 6 n. 26, p. 22048-22059-
dc.identifier.issn1949-2553-
dc.identifier.urihttp://hdl.handle.net/10722/215048-
dc.description.abstractMicroRNAs are differentially expressed in breast cancer cells and have been implicated in cancer formation, tumour invasion and metastasis. We investigated the miRNA expression profiles in the developing mammary gland. MiR-137 was expressed prominently in the developing mammary gland. When the miR-137 was over-expressed in the embryo, the mammary epithelium became thickened. Moreover, genes associated with mammary gland formation such as Tbx3 and Lef1 were not expressed. This suggests that miR-137 induces gland formation and invasion. When miR-137 was over-expressed in MDA-MB-231 cells, their ability to form tumours in adult mice was significantly reduced. These data support miR-137 decides epithelial cell behavior in the human breast cancer. It also suggests that miR-137 is a potential therapeutic target for amelioration of breast cancer progression.-
dc.languageeng-
dc.publisherImpact Journals LLC. The Journal's web site is located at http://www.impactjournals.com/oncotarget/index.html-
dc.relation.ispartofOncotarget-
dc.rightsThe final published version is available online at http://dx.doi.org/10.18632/oncotarget.4218-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectBreast cancer-
dc.subjectMammary gland development-
dc.subjectMiR-137-
dc.subjectTachykinin-1-
dc.subjectTumour suppressor-
dc.titleA contrasting function for miR-137 in embryonic mammogenesis and adult breast carcinogenesis-
dc.typeArticle-
dc.identifier.emailJung, HS: hsjung@hku.hk-
dc.identifier.authorityJung, HS=rp01683-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.18632/oncotarget.4218-
dc.identifier.pmid26215676-
dc.identifier.pmcidPMC4673145-
dc.identifier.scopuseid_2-s2.0-84941236552-
dc.identifier.hkuros248206-
dc.identifier.volume6-
dc.identifier.issue26-
dc.identifier.spage22048-
dc.identifier.epage22059-
dc.identifier.isiWOS:000362954800039-
dc.publisher.placeUnited States-
dc.identifier.issnl1949-2553-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats