id paper:paper_00085472_v78_n16_p4497_Tocci
record_format dspace
spelling paper:paper_00085472_v78_n16_p4497_Tocci2023-06-08T14:32:09Z R-Spondin3 is associated with basal-progenitor behavior in normal and tumor mammary cells G protein coupled receptor leucine rich repeat containing G protein coupled receptor protein R spondin3 transcription factor RUNX unclassified drug adult animal cell animal experiment animal model animal tissue Article basal like breast cancer breast carcinogenesis breast cell cancer cell cancer growth cell differentiation cell migration controlled study epithelial mesenchymal transition female gene gene knockdown gene overexpression gene targeting human human cell human tissue in vivo study mouse nonhuman priority journal protein expression RSPO3 gene stem cell Wnt signaling R-spondin3 (RSPO3) is a member of a family of secreted proteins that enhance Wnt signaling pathways in diverse processes, including cancer. However, the role of RSPO3 in mammary gland and breast cancer development remains unclear. In this study, we show that RSPO3 is expressed in the basal stem cell–enriched compartment of normal mouse mammary glands but is absent from committed mature luminal cells in which exogenous RSPO3 impairs lactogenic differentiation. RSPO3 knockdown in basal-like mouse mammary tumor cells reduced canonical Wnt signaling, epithelial-to-mesenchymal transition-like features, migration capacity, and tumor formation in vivo. Conversely, RSPO3 overexpression, which was associated with some LGR and RUNX factors, highly correlated with the basal-like subtype among patients with breast cancer. Thus, we identified RSPO3 as a novel key modulator of breast cancer development and a potential target for treatment of basal-like breast cancers. Significance: These findings identify RSPO3 as a potential therapetuic target in basal-like breast cancers. Graphical Abstract: http://cancerres.aacrjournals.org/content/canres/78/16/4497/F1.large.jpg. 2018 American Association for Cancer Research. 2018 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00085472_v78_n16_p4497_Tocci http://hdl.handle.net/20.500.12110/paper_00085472_v78_n16_p4497_Tocci
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-134
collection Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic G protein coupled receptor
leucine rich repeat containing G protein coupled receptor
protein
R spondin3
transcription factor RUNX
unclassified drug
adult
animal cell
animal experiment
animal model
animal tissue
Article
basal like breast cancer
breast carcinogenesis
breast cell
cancer cell
cancer growth
cell differentiation
cell migration
controlled study
epithelial mesenchymal transition
female
gene
gene knockdown
gene overexpression
gene targeting
human
human cell
human tissue
in vivo study
mouse
nonhuman
priority journal
protein expression
RSPO3 gene
stem cell
Wnt signaling
spellingShingle G protein coupled receptor
leucine rich repeat containing G protein coupled receptor
protein
R spondin3
transcription factor RUNX
unclassified drug
adult
animal cell
animal experiment
animal model
animal tissue
Article
basal like breast cancer
breast carcinogenesis
breast cell
cancer cell
cancer growth
cell differentiation
cell migration
controlled study
epithelial mesenchymal transition
female
gene
gene knockdown
gene overexpression
gene targeting
human
human cell
human tissue
in vivo study
mouse
nonhuman
priority journal
protein expression
RSPO3 gene
stem cell
Wnt signaling
R-Spondin3 is associated with basal-progenitor behavior in normal and tumor mammary cells
topic_facet G protein coupled receptor
leucine rich repeat containing G protein coupled receptor
protein
R spondin3
transcription factor RUNX
unclassified drug
adult
animal cell
animal experiment
animal model
animal tissue
Article
basal like breast cancer
breast carcinogenesis
breast cell
cancer cell
cancer growth
cell differentiation
cell migration
controlled study
epithelial mesenchymal transition
female
gene
gene knockdown
gene overexpression
gene targeting
human
human cell
human tissue
in vivo study
mouse
nonhuman
priority journal
protein expression
RSPO3 gene
stem cell
Wnt signaling
description R-spondin3 (RSPO3) is a member of a family of secreted proteins that enhance Wnt signaling pathways in diverse processes, including cancer. However, the role of RSPO3 in mammary gland and breast cancer development remains unclear. In this study, we show that RSPO3 is expressed in the basal stem cell–enriched compartment of normal mouse mammary glands but is absent from committed mature luminal cells in which exogenous RSPO3 impairs lactogenic differentiation. RSPO3 knockdown in basal-like mouse mammary tumor cells reduced canonical Wnt signaling, epithelial-to-mesenchymal transition-like features, migration capacity, and tumor formation in vivo. Conversely, RSPO3 overexpression, which was associated with some LGR and RUNX factors, highly correlated with the basal-like subtype among patients with breast cancer. Thus, we identified RSPO3 as a novel key modulator of breast cancer development and a potential target for treatment of basal-like breast cancers. Significance: These findings identify RSPO3 as a potential therapetuic target in basal-like breast cancers. Graphical Abstract: http://cancerres.aacrjournals.org/content/canres/78/16/4497/F1.large.jpg. 2018 American Association for Cancer Research.
title R-Spondin3 is associated with basal-progenitor behavior in normal and tumor mammary cells
title_short R-Spondin3 is associated with basal-progenitor behavior in normal and tumor mammary cells
title_full R-Spondin3 is associated with basal-progenitor behavior in normal and tumor mammary cells
title_fullStr R-Spondin3 is associated with basal-progenitor behavior in normal and tumor mammary cells
title_full_unstemmed R-Spondin3 is associated with basal-progenitor behavior in normal and tumor mammary cells
title_sort r-spondin3 is associated with basal-progenitor behavior in normal and tumor mammary cells
publishDate 2018
url https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00085472_v78_n16_p4497_Tocci
http://hdl.handle.net/20.500.12110/paper_00085472_v78_n16_p4497_Tocci
_version_ 1768541919711854592