Interaction between IGF-IR and ER Induced by E2 and IGF-I

Estrogen receptor (ER) is a nuclear receptor and the insulin-like growth factor-I (IGF-I) receptor (IGF-IR) is a transmembrane tyrosine kinase receptor. Estrogen and IGF-I are known to have synergistic effects on the growth of breast cancer cells. Recently, non-nuclear effects of ER have been under...

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Main Authors:	Yu, Zhenghong, Gao, Weimin, Jiang, Enze, Lu, Fang, Zhang, Luo, Shi, Zhaorong, Wang, Xinxing, Chen, Longbang, Lv, Tangfeng
Format:	Online
Language:	English
Published:	Public Library of Science 2013
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3660452/

id	pubmed-3660452
recordtype	oai_dc
spelling	pubmed-36604522013-05-23 Interaction between IGF-IR and ER Induced by E2 and IGF-I Yu, Zhenghong Gao, Weimin Jiang, Enze Lu, Fang Zhang, Luo Shi, Zhaorong Wang, Xinxing Chen, Longbang Lv, Tangfeng Research Article Estrogen receptor (ER) is a nuclear receptor and the insulin-like growth factor-I (IGF-I) receptor (IGF-IR) is a transmembrane tyrosine kinase receptor. Estrogen and IGF-I are known to have synergistic effects on the growth of breast cancer cells. Recently, non-nuclear effects of ER have been under investigation. To study the mechanism involved in this process, we have used MCF-7 breast cancer cell lines transfected with IGF-IR anti-sense cDNA (SX13, MCF-7SX13) that resulted in 50% reduction of IGF-IR. In MCF-7 cells, estradiol (E2) and IGF-I induced the rapid association of ER to IGF-IR, however, the interaction was abrogated in MCF-7SX13 cells. In addition, NWTB3 cells (NIH3T3 cells overexpressing IGF-IR) were transiently transfected with ERα, the ER-IGF-IR interaction was induced by both E2 and IGF-I. Moreover, ERα regulated the IGF-I signaling pathways through phosphorylation of ERK1/2 and Akt and the interaction of ER-IGF-IR potentiated the cell growth. Finally, E2 and IGF-I stimulated translocation of ER from the nucleus to the cytoplasm. Taken together, these findings reveal that the interaction of the ER and IGF-IR is important for the non-genomic effects of ER. Public Library of Science 2013-05-21 /pmc/articles/PMC3660452/ /pubmed/23704881 http://dx.doi.org/10.1371/journal.pone.0062642 Text en © 2013 Yu et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Yu, Zhenghong Gao, Weimin Jiang, Enze Lu, Fang Zhang, Luo Shi, Zhaorong Wang, Xinxing Chen, Longbang Lv, Tangfeng
spellingShingle	Yu, Zhenghong Gao, Weimin Jiang, Enze Lu, Fang Zhang, Luo Shi, Zhaorong Wang, Xinxing Chen, Longbang Lv, Tangfeng Interaction between IGF-IR and ER Induced by E2 and IGF-I
author_facet	Yu, Zhenghong Gao, Weimin Jiang, Enze Lu, Fang Zhang, Luo Shi, Zhaorong Wang, Xinxing Chen, Longbang Lv, Tangfeng
author_sort	Yu, Zhenghong
title	Interaction between IGF-IR and ER Induced by E2 and IGF-I
title_short	Interaction between IGF-IR and ER Induced by E2 and IGF-I
title_full	Interaction between IGF-IR and ER Induced by E2 and IGF-I
title_fullStr	Interaction between IGF-IR and ER Induced by E2 and IGF-I
title_full_unstemmed	Interaction between IGF-IR and ER Induced by E2 and IGF-I
title_sort	interaction between igf-ir and er induced by e2 and igf-i
description	Estrogen receptor (ER) is a nuclear receptor and the insulin-like growth factor-I (IGF-I) receptor (IGF-IR) is a transmembrane tyrosine kinase receptor. Estrogen and IGF-I are known to have synergistic effects on the growth of breast cancer cells. Recently, non-nuclear effects of ER have been under investigation. To study the mechanism involved in this process, we have used MCF-7 breast cancer cell lines transfected with IGF-IR anti-sense cDNA (SX13, MCF-7SX13) that resulted in 50% reduction of IGF-IR. In MCF-7 cells, estradiol (E2) and IGF-I induced the rapid association of ER to IGF-IR, however, the interaction was abrogated in MCF-7SX13 cells. In addition, NWTB3 cells (NIH3T3 cells overexpressing IGF-IR) were transiently transfected with ERα, the ER-IGF-IR interaction was induced by both E2 and IGF-I. Moreover, ERα regulated the IGF-I signaling pathways through phosphorylation of ERK1/2 and Akt and the interaction of ER-IGF-IR potentiated the cell growth. Finally, E2 and IGF-I stimulated translocation of ER from the nucleus to the cytoplasm. Taken together, these findings reveal that the interaction of the ER and IGF-IR is important for the non-genomic effects of ER.
publisher	Public Library of Science
publishDate	2013
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3660452/
_version_	1611979876518068224

Interaction between IGF-IR and ER Induced by E2 and IGF-I

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