國家衛生研究院 NHRI:Item 3990099045/6231

NHRI > Institute of Cellular and Systems Medicine > Yasuhisa Fukui(2010-2016) > Periodical Articles > Item 3990099045/6231

Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/6231

Title:	Heregulin beta-1 induces loss of Cell-Cell contact and enhances expression of MUC1 at the cell surface in HCC2998 and MKN45-1 cells
Other Titles:	Heregulin β-1 induces loss of Cell-Cell contact and enhances expression of MUC1 at the cell surface in HCC2998 and MKN45-1 cells
Authors:	Okoshi, R;Shu, CL;Ihara, S;Fukui, Y
Contributors:	Institute of Cellular and Systems Medicine
Abstract:	Signal transduction and cell responses after stimulation with heregulin β-1 (HRG) are examined in HCC2998 and MKN45-1 cells, which have been used for a model system to study the formation of signet ring carcinomas, one of poorly differentiated adenocarcinomas. HRG stimulation causes rounding of the cells, responding to HRG. The adherens junction, which is present in the control cells, is disrupted and cell-cell interaction is lost after stimulation. Inhibition of phosphatidylinositol (PI)-3 kinase or p38 MAP kinase blocked this reaction, which indicates that the PI-3 kinase-p38 MAP kinase pathway is required for this reaction. Inhibition of the p38 MAP kinase pathway resulted in immediate restoration of cell-cell interaction. This result indicates that signaling for adherent molecules is strictly regulated by growth factor signaling. Expression of MUC1 at the cell surface is also observed and found to be expressed only after HRG stimulation. The total amount of MUC1 remains unchanged, suggesting that this amount is not due to induction of gene expression but to translocation of MUC1 from the inner membrane to the plasma membrane. This reaction is independent of the cytohesin pathway but dependent on PI-3 kinase activity. In addition to these reactions, HRG stimulates cell growth of both HCC2998 and MKN45-1 cells, depending on the ERK pathway given that the MEK inhibitor abolishes this effect. Therefore, HRG induces various reactions in HCC2998 and MKN45-1 cells by different pathways. These reactions are all related to characteristics of tumors, which implicates that HRG signaling can contribute to the formation of tumors.
Date:	2011-12
Relation:	PLoS ONE. 2011 Dec;6(12):Article number e29599.
Link to:	http://dx.doi.org/10.1371/journal.pone.0029599
JIF/Ranking 2023:	http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=1932-6203&DestApp=IC2JCR
Cited Times(WOS):	https://www.webofscience.com/wos/woscc/full-record/WOS:000299684700073
Cited Times(Scopus):	http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84055216991
Appears in Collections:	[Yasuhisa Fukui(2010-2016)] Periodical Articles

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