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dc.contributor.authorLiu, Wensheng
dc.contributor.authorKovacevic, Zaklina
dc.contributor.authorPeng, Zhihai
dc.contributor.authorJin, Runsen
dc.contributor.authorWang, Puxiongzhi
dc.contributor.authorYue, Fei
dc.contributor.authorZheng, Minhua
dc.contributor.authorHuang, Michael L-H
dc.contributor.authorJansson, Patric J
dc.contributor.authorRichardson, Vera
dc.contributor.authorKalinowski, Danuta S
dc.contributor.authorLane, Darius JR
dc.contributor.authorMerlot, Angelica M
dc.contributor.authorSahni, Sumit
dc.contributor.authorRichardson, Des R
dc.date.accessioned2021-04-30T01:38:44Z
dc.date.available2021-04-30T01:38:44Z
dc.date.issued2015
dc.identifier.issn1949-2553
dc.identifier.doi10.18632/oncotarget.5849
dc.identifier.urihttp://hdl.handle.net/10072/404054
dc.description.abstractA major problem for cancer patients is the metastasis of cancer cells from the primary tumor. This involves: (1) migration through the basement membrane; (2) dissemination via the circulatory system; and (3) invasion into a secondary site. Metastasis suppressors, by definition, inhibit metastasis at any step of the metastatic cascade. Notably, Src is a non-receptor, cytoplasmic, tyrosine kinase, which becomes aberrantly activated in many cancer-types following stimulation of plasma membrane receptors (e.g., receptor tyrosine kinases and integrins). There is evidence of a prominent role of Src in tumor progression-related events such as the epithelial-mesenchymal transition (EMT) and the development of metastasis. However, the precise molecular interactions of Src with metastasis suppressors remain unclear. Herein, we review known metastasis suppressors and summarize recent advances in understanding the mechanisms of how these proteins inhibit metastasis through modulation of Src. Particular emphasis is bestowed on the potent metastasis suppressor, N-myc downstream regulated gene 1 (NDRG1) and its interactions with the Src signaling cascade. Recent studies demonstrated a novel mechanism through which NDRG1 plays a significant role in regulating cancer cell migration by inhibiting Src activity. Moreover, we discuss the rationale for targeting metastasis suppressor genes as a sound therapeutic modality, and we review several examples from the literature where such strategies show promise. Collectively, this review summarizes the essential interactions of metastasis suppressors with Src and their effects on progression of cancer metastasis. Moreover, interesting unresolved issues regarding these proteins as well as their potential as therapeutic targets are also discussed.
dc.description.peerreviewedYes
dc.languageEnglish
dc.publisherImpact Journals, LLC
dc.relation.ispartofpagefrom35522
dc.relation.ispartofpageto35541
dc.relation.ispartofissue34
dc.relation.ispartofjournalOncotarget
dc.relation.ispartofvolume6
dc.subject.fieldofresearchOncology and carcinogenesis
dc.subject.fieldofresearchcode3211
dc.subject.keywordsScience & Technology
dc.subject.keywordsLife Sciences & Biomedicine
dc.subject.keywordsCell Biology
dc.subject.keywordsmetastasis suppressor
dc.titleThe molecular effect of metastasis suppressors on Src signaling and tumorigenesis: new therapeutic targets
dc.typeJournal article
dc.type.descriptionC1 - Articles
dcterms.bibliographicCitationLiu, W; Kovacevic, Z; Peng, Z; Jin, R; Wang, P; Yue, F; Zheng, M; Huang, ML-H; Jansson, PJ; Richardson, V; Kalinowski, DS; Lane, DJR; Merlot, AM; Sahni, S; Richardson, DR, The molecular effect of metastasis suppressors on Src signaling and tumorigenesis: new therapeutic targets, Oncotarget, 2015, 6 (34), pp. 35522-35541
dcterms.dateAccepted2015-08-15
dcterms.licensehttp://creativecommons.org/licenses/by/3.0/
dc.date.updated2021-04-30T01:36:48Z
dc.description.versionVersion of Record (VoR)
gro.rights.copyright© The Author(s) 2015. This is an Open Access article distributed under the terms of the Creative Commons Attribution 3.0 Unported (CC BY 3.0) License (http://creativecommons.org/licenses/by/3.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
gro.hasfulltextFull Text
gro.griffith.authorRichardson, Des R.


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