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Article ; Online: Retraction Note to: Roles of MicroRNAs and Other Non-coding RNAs in Breast Cancer Metastasis.

Valastyan, Scott

Journal of mammary gland biology and neoplasia

2016 Volume 21, Issue 3-4, Page(s) 151

Language	English
Publishing date	2016
Publishing country	United States
Document type	Journal Article ; Retraction of Publication
ZDB-ID	1327345-0
ISSN	1573-7039 ; 1083-3021
ISSN (online)	1573-7039
ISSN	1083-3021
DOI	10.1007/s10911-016-9360-9
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Zs.A 4478: Show issues

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Article ; Online: Endogenous anticancer mechanisms: metastasis.

Valastyan, Scott

Frontiers in bioscience (Elite edition)

2012 Volume 4, Issue 5, Page(s) 1888–1897

Abstract: Metastases, rather than the primary tumors from which these malignant growths are spawned, are culpable for greater than 90 % of human cancer-associated mortality. Metastases arise through the completion of a series of cell-biological events - ... ...

Abstract	Metastases, rather than the primary tumors from which these malignant growths are spawned, are culpable for greater than 90 % of human cancer-associated mortality. Metastases arise through the completion of a series of cell-biological events - collectively termed "the invasion-metastasis cascade" - which involve the dissemination of tumor cells to distant organ sites and their subsequent adaptation to these foreign microenvironments. Importantly, a number of endogenous mechanisms exist that serve to prevent metastatic progression. These safeguards must be overcome by incipient metastatic tumor cells in order for them to generate detectable metastases. Here, I highlight four endogenous mechanisms that protect against the development of metastatic disease in breast carcinomas. I discuss how the expression of these genes are dampened during malignant progression, the downstream responses they orchestrate, and clinical opportunities to therapeutically target these mechanisms. Indeed, one potentially effective strategy for the remediation of metastatic disease involves the reactivation of endogenous anti-metastasis mechanisms. Therefore, knowledge regarding endogenous anti-metastasis mechanisms may both further our comprehension of the basic etiology of metastasis and also guide the treatment of human tumors.
MeSH term(s)	Animals ; Cadherins/physiology ; Humans ; MicroRNAs/physiology ; NM23 Nucleoside Diphosphate Kinases/physiology ; Neoplasm Invasiveness ; Neoplasm Metastasis
Chemical Substances	Cadherins ; MicroRNAs ; NM23 Nucleoside Diphosphate Kinases ; NME1 protein, human (EC 2.7.4.6)
Language	English
Publishing date	2012-01-01
Publishing country	Singapore
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	2565080-4
ISSN	1945-0508 ; 1945-0494
ISSN (online)	1945-0508
ISSN	1945-0494
DOI	10.2741/e510
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Article ; Online: Roles of microRNAs and other non-coding RNAs in breast cancer metastasis.

Valastyan, Scott

publication RETRACTED

Journal of mammary gland biology and neoplasia

2012 Volume 17, Issue 1, Page(s) 23–32

Abstract: Despite the fact that metastases are responsible for the overwhelming majority of human cancer deaths, our comprehension of the molecular events that drive metastatic progression remains woefully incomplete. Excitingly, the recent appreciation that ... ...

Abstract	Despite the fact that metastases are responsible for the overwhelming majority of human cancer deaths, our comprehension of the molecular events that drive metastatic progression remains woefully incomplete. Excitingly, the recent appreciation that various species of non-coding RNAs—including microRNAs—play pivotal roles in dictating the malignant behaviors of breast carcinoma cells promises to afford new insights into the molecular circuitry that determines metastatic propensity. Here, I summarize our current knowledge regarding these still-emerging functions for non-coding RNAs in the pathogenesis of breast cancer metastasis, with an emphasis placed upon the roles played by microRNAs in these processes. Additionally, I discuss the potential translational opportunities afforded by these research findings for the diagnosis and treatment of human breast tumors. When assessed collectively, it is apparent that although this field of research is still in its infancy, comprehension of the biological actions of microRNAs and other non-coding RNAs will hold important consequences for our understanding of the etiology of metastatic disease, as well as its clinical management and treatment.
MeSH term(s)	Animals ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; MicroRNAs/genetics ; Neoplasm Metastasis ; RNA, Untranslated/genetics
Chemical Substances	MicroRNAs ; RNA, Untranslated
Language	English
Publishing date	2012-01-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review ; Retracted Publication
ZDB-ID	1327345-0
ISSN	1573-7039 ; 1083-3021
ISSN (online)	1573-7039
ISSN	1083-3021
DOI	10.1007/s10911-012-9241-9
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Tumor metastasis: molecular insights and evolving paradigms.

Valastyan, Scott / Weinberg, Robert A

Cell

2011 Volume 147, Issue 2, Page(s) 275–292

Abstract: Metastases represent the end products of a multistep cell-biological process termed the invasion-metastasis cascade, which involves dissemination of cancer cells to anatomically distant organ sites and their subsequent adaptation to foreign tissue ... ...

Abstract	Metastases represent the end products of a multistep cell-biological process termed the invasion-metastasis cascade, which involves dissemination of cancer cells to anatomically distant organ sites and their subsequent adaptation to foreign tissue microenvironments. Each of these events is driven by the acquisition of genetic and/or epigenetic alterations within tumor cells and the co-option of nonneoplastic stromal cells, which together endow incipient metastatic cells with traits needed to generate macroscopic metastases. Recent advances provide provocative insights into these cell-biological and molecular changes, which have implications regarding the steps of the invasion-metastasis cascade that appear amenable to therapeutic targeting.
MeSH term(s)	Animals ; Basement Membrane/pathology ; Humans ; Neoplasm Invasiveness/pathology ; Neoplasm Metastasis/drug therapy ; Neoplasm Metastasis/pathology ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/pathology ; Prognosis ; Signal Transduction ; Stromal Cells/pathology
Language	English
Publishing date	2011-10-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2011.09.024
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Zs.A 1167: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 58: Show issues

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Article ; Online: Roles for microRNAs in the regulation of cell adhesion molecules.

Valastyan, Scott / Weinberg, Robert A

Journal of cell science

2011 Volume 124, Issue Pt 7, Page(s) 999–1006

Abstract: Maintenance of appropriate cell adhesion is crucial for normal cellular and organismal homeostasis. Certain microRNAs have recently been found capable of regulating molecules that oversee the fundamental cell biological events that drive cellular ... ...

Abstract	Maintenance of appropriate cell adhesion is crucial for normal cellular and organismal homeostasis. Certain microRNAs have recently been found capable of regulating molecules that oversee the fundamental cell biological events that drive cellular adhesion. It is now apparent that microRNAs play crucial roles in the great majority of biochemical pathways that contribute to normal cell adhesion. In this Commentary, we describe the latest advances within this still-emerging field, and highlight connections between the deregulation of microRNAs that affect cell-adhesion-associated molecules and the pathogenesis of several human diseases. Current evidence suggests that the ability of certain microRNAs--notably miR-17, miR-29, miR-31, miR-124 and miR-200--to pleiotropically regulate multiple molecular components of the cell adhesion machinery endows these microRNAs with the capacity to function as key modulators of adhesion-associated processes. This, in turn, holds important implications for our understanding of both the basic biology of cell adhesion and the etiology of multiple pathological conditions.
MeSH term(s)	Animals ; Cell Adhesion ; Cell Adhesion Molecules/genetics ; Cell Adhesion Molecules/metabolism ; Humans ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/physiopathology
Chemical Substances	Cell Adhesion Molecules ; MicroRNAs
Language	English
Publishing date	2011-03-14
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2993-2
ISSN	1477-9137 ; 0021-9533
ISSN (online)	1477-9137
ISSN	0021-9533
DOI	10.1242/jcs.081513
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Zs.A 1200: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 14: Show issues

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Article ; Online: Metastasis suppression: a role of the Dice(r).

Valastyan, Scott / Weinberg, Robert A

Genome biology

2010 Volume 11, Issue 11, Page(s) 141

Abstract: Recent studies have implicated the microRNA biogenesis enzyme Dicer as a suppressor of breast carcinoma metastasis and elucidated upstream signaling pathways that control Dicer levels. ...

Abstract	Recent studies have implicated the microRNA biogenesis enzyme Dicer as a suppressor of breast carcinoma metastasis and elucidated upstream signaling pathways that control Dicer levels.
MeSH term(s)	Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Genes, Suppressor ; Humans ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Neoplasm Metastasis/genetics ; Ribonuclease III/genetics ; Ribonuclease III/metabolism ; Signal Transduction ; Trans-Activators/genetics ; Trans-Activators/metabolism ; Transcription Factors ; Tumor Suppressor Proteins/genetics ; Tumor Suppressor Proteins/metabolism ; Up-Regulation
Chemical Substances	MicroRNAs ; TP63 protein, human ; Trans-Activators ; Transcription Factors ; Tumor Suppressor Proteins ; Ribonuclease III (EC 3.1.26.3)
Language	English
Publishing date	2010-11-30
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2040529-7
ISSN	1474-760X ; 1474-760X
ISSN (online)	1474-760X
ISSN	1474-760X
DOI	10.1186/gb-2010-11-11-141
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: miR-31: a crucial overseer of tumor metastasis and other emerging roles.

Valastyan, Scott / Weinberg, Robert A

Cell cycle (Georgetown, Tex.)

2010 Volume 9, Issue 11, Page(s) 2124–2129

Abstract: MicroRNAs constitute a family of pleiotropically acting short regulatory RNAs. Increasingly, specific microRNAs have been implicated as key modulators of a variety of normal physiologic processes; moreover, the aberrant activity of certain microRNAs has ... ...

Abstract	MicroRNAs constitute a family of pleiotropically acting short regulatory RNAs. Increasingly, specific microRNAs have been implicated as key modulators of a variety of normal physiologic processes; moreover, the aberrant activity of certain microRNAs has been linked to the pathogenesis of multiple diseases. The microRNA miR-31 has been identified as a crucial overseer of several normal and diseased phenotypes. Here, we describe current knowledge regarding the functions of miR-31, with an emphasis placed upon the role of this microRNA in neoplastic development and tumor metastasis. Additionally, we highlight a number of recent reports concerning the contributions of miR-31 to other pathological states, the role of this microRNA in normal physiology, and the upstream mechanisms by which miR-31 expression levels are regulated. Assessed collectively, existing evidence suggests that miR-31 concomitantly regulates a number of essential signaling pathways in mammalian cells. For these reasons, further elucidation of the biological actions of miR-31 may prove significant for the prognosis and remediation of various pathological states.
MeSH term(s)	Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Female ; Humans ; MicroRNAs/metabolism ; MicroRNAs/physiology ; Neoplasm Metastasis ; Signal Transduction
Chemical Substances	MIRN31 microRNA, human ; MicroRNAs
Language	English
Publishing date	2010-06-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	2146183-1
ISSN	1551-4005 ; 1538-4101 ; 1554-8627
ISSN (online)	1551-4005
ISSN	1538-4101 ; 1554-8627
DOI	10.4161/cc.9.11.11843
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Zs.A 5881: Show issues

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Article: Metastasis suppression: a role of the Dice(r)

Valastyan, Scott / Weinberg, Robert A

Genome biology. 2010 Nov., v. 11, no. 11

2010

Abstract: Recent studies have implicated the microRNA biogenesis enzyme Dicer as a suppressor of breast carcinoma metastasis and elucidated upstream signaling pathways that control Dicer levels. ...

Abstract	Recent studies have implicated the microRNA biogenesis enzyme Dicer as a suppressor of breast carcinoma metastasis and elucidated upstream signaling pathways that control Dicer levels.
Keywords	biogenesis ; breast neoplasms ; metastasis ; microRNA ; signal transduction
Language	English
Dates of publication	2010-11
Size	p. 141.
Publishing place	BioMed Central
Document type	Article
ZDB-ID	2040529-7
ISSN	1474-760X ; 1465-6914 ; 1465-6906
ISSN (online)	1474-760X ; 1465-6914
ISSN	1465-6906
DOI	10.1186/gb-2010-11-11-141
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Assaying microRNA loss-of-function phenotypes in mammalian cells: emerging tools and their potential therapeutic utility.

Valastyan, Scott / Weinberg, Robert A

RNA biology

2009 Volume 6, Issue 5, Page(s) 541–545

Abstract: MicroRNAs are small, non-coding RNAs that are increasingly appreciated to play critical roles in the modulation of gene expression. In mammalian cells, our knowledge regarding the full impact of microRNAs on cellular behavior remains fragmentary. This ... ...

Abstract	MicroRNAs are small, non-coding RNAs that are increasingly appreciated to play critical roles in the modulation of gene expression. In mammalian cells, our knowledge regarding the full impact of microRNAs on cellular behavior remains fragmentary. This has been due, in significant part, to the limited availability of experimental tools for studying microRNA loss-of-function phenotypes. Recently, several strategies for achieving this goal have been developed. Here, we discuss these methodologies for inhibiting specific microRNAs in mammalian cells both in vitro and in vivo, compare and contrast the strengths and weaknesses of these approaches, and speculate regarding the future impact of these antagonists on the treatment of human diseases such as cancer. These emerging techniques enable the attenuation of microRNA function in a manner that is quite sequence-specific, relatively long-lasting and increasingly cost-effective. As such, some of these advances hold great promise in terms of their eventual utility as therapeutic agents.
MeSH term(s)	Animals ; Cells ; Drug Therapy ; Humans ; MicroRNAs/antagonists & inhibitors ; Neoplasms/drug therapy
Chemical Substances	MicroRNAs
Language	English
Publishing date	2009-11-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ISSN	1555-8584
ISSN (online)	1555-8584
DOI	10.4161/rna.6.5.10081
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: MicroRNAs: Crucial multi-tasking components in the complex circuitry of tumor metastasis.

Valastyan, Scott / Weinberg, Robert A

Cell cycle (Georgetown, Tex.)

2009 Volume 8, Issue 21, Page(s) 3506–3512

Abstract: Distant metastases are the underlying cause of patient mortality in an overwhelming majority of human carcinomas. Certain microRNAs have recently been found capable of regulating the process of tumor metastasis. In this review, we highlight advances ... ...

Abstract	Distant metastases are the underlying cause of patient mortality in an overwhelming majority of human carcinomas. Certain microRNAs have recently been found capable of regulating the process of tumor metastasis. In this review, we highlight advances within this rapidly emerging field, endeavor to connect known microRNA pathways with recent conceptual advances in the larger field of metastasis research, and speculate regarding the future utility of microRNAs in the diagnosis and treatment of human cancers. Assessed collectively, current evidence suggests that the pleiotropic activities of microRNAs endow them with the capacity to function as crucial, yet previously unappreciated, nodes within already-identified metastasis regulatory circuitry. This has important implications for our understanding of the pathogenesis of high-grade malignancies.
MeSH term(s)	Humans ; Hyaluronan Receptors/genetics ; Hyaluronan Receptors/metabolism ; MicroRNAs/metabolism ; MicroRNAs/therapeutic use ; Neoplasm Metastasis/diagnosis ; Neoplasm Metastasis/genetics ; Neoplasm Metastasis/therapy ; SOXC Transcription Factors/antagonists & inhibitors ; SOXC Transcription Factors/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism
Chemical Substances	CD44 protein, human ; Hyaluronan Receptors ; MicroRNAs ; SOX4 protein, human ; SOXC Transcription Factors ; Transcription Factors
Language	English
Publishing date	2009-11-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	2146183-1
ISSN	1551-4005 ; 1538-4101 ; 1554-8627
ISSN (online)	1551-4005
ISSN	1538-4101 ; 1554-8627
DOI	10.4161/cc.8.21.9802
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