Notch signaling activation suppresses v-Src-induced transformation of neural cells by restoring TGF-β-mediated differentiation.

<h4>Background</h4>We have been investigating how interruption of differentiation contributes to the oncogenic process and the possibility to reverse the transformed phenotype by restoring differentiation. In a previous report, we correlated the capacity of intracellular Notch (ICN) to s...

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Autores principales:	Samira Amarir, Maria Marx, Georges Calothy
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2010
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/7fba7fad70cf42549f9ae25864c66221
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spelling	oai:doaj.org-article:7fba7fad70cf42549f9ae25864c662212021-11-18T07:02:59ZNotch signaling activation suppresses v-Src-induced transformation of neural cells by restoring TGF-β-mediated differentiation.1932-620310.1371/journal.pone.0013572https://doaj.org/article/7fba7fad70cf42549f9ae25864c662212010-10-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21042581/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>We have been investigating how interruption of differentiation contributes to the oncogenic process and the possibility to reverse the transformed phenotype by restoring differentiation. In a previous report, we correlated the capacity of intracellular Notch (ICN) to suppress v-Src-mediated transformation of quail neuroretina (QNR/v-src(ts)) cells with the acquisition by these undifferentiated cells of glial differentiation markers.<h4>Methodology/principal findings</h4>In this work, we have identified autocrine TGF-β3 signaling activation as a major effector of Notch-induced phenotypic changes, sufficient to induce transition in differentiation markers expression, suppress morphological transformation and significantly inhibit anchorage-independent growth. We also show that this signaling is constitutive of and contributes to ex-vivo autonomous QNR cell differentiation and that its down-regulation is essential to achieve v-Src-induced transformation.<h4>Conclusions/significance</h4>These results support the possibility that Notch signaling induces differentiation and suppresses transformation by a novel mechanism, involving secreted proteins. They also underline the importance of extracellular signals in controlling the balance between normal and transformed phenotypes.Samira AmarirMaria MarxGeorges CalothyPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 5, Iss 10, p e13572 (2010)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Samira Amarir Maria Marx Georges Calothy Notch signaling activation suppresses v-Src-induced transformation of neural cells by restoring TGF-β-mediated differentiation.
description	<h4>Background</h4>We have been investigating how interruption of differentiation contributes to the oncogenic process and the possibility to reverse the transformed phenotype by restoring differentiation. In a previous report, we correlated the capacity of intracellular Notch (ICN) to suppress v-Src-mediated transformation of quail neuroretina (QNR/v-src(ts)) cells with the acquisition by these undifferentiated cells of glial differentiation markers.<h4>Methodology/principal findings</h4>In this work, we have identified autocrine TGF-β3 signaling activation as a major effector of Notch-induced phenotypic changes, sufficient to induce transition in differentiation markers expression, suppress morphological transformation and significantly inhibit anchorage-independent growth. We also show that this signaling is constitutive of and contributes to ex-vivo autonomous QNR cell differentiation and that its down-regulation is essential to achieve v-Src-induced transformation.<h4>Conclusions/significance</h4>These results support the possibility that Notch signaling induces differentiation and suppresses transformation by a novel mechanism, involving secreted proteins. They also underline the importance of extracellular signals in controlling the balance between normal and transformed phenotypes.
format	article
author	Samira Amarir Maria Marx Georges Calothy
author_facet	Samira Amarir Maria Marx Georges Calothy
author_sort	Samira Amarir
title	Notch signaling activation suppresses v-Src-induced transformation of neural cells by restoring TGF-β-mediated differentiation.
title_short	Notch signaling activation suppresses v-Src-induced transformation of neural cells by restoring TGF-β-mediated differentiation.
title_full	Notch signaling activation suppresses v-Src-induced transformation of neural cells by restoring TGF-β-mediated differentiation.
title_fullStr	Notch signaling activation suppresses v-Src-induced transformation of neural cells by restoring TGF-β-mediated differentiation.
title_full_unstemmed	Notch signaling activation suppresses v-Src-induced transformation of neural cells by restoring TGF-β-mediated differentiation.
title_sort	notch signaling activation suppresses v-src-induced transformation of neural cells by restoring tgf-β-mediated differentiation.
publisher	Public Library of Science (PLoS)
publishDate	2010
url	https://doaj.org/article/7fba7fad70cf42549f9ae25864c66221
work_keys_str_mv	AT samiraamarir notchsignalingactivationsuppressesvsrcinducedtransformationofneuralcellsbyrestoringtgfbmediateddifferentiation AT mariamarx notchsignalingactivationsuppressesvsrcinducedtransformationofneuralcellsbyrestoringtgfbmediateddifferentiation AT georgescalothy notchsignalingactivationsuppressesvsrcinducedtransformationofneuralcellsbyrestoringtgfbmediateddifferentiation
_version_	1718423987920306176

Notch signaling activation suppresses v-Src-induced transformation of neural cells by restoring TGF-β-mediated differentiation.

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