S100A4 released from highly bone-metastatic breast cancer cells plays a critical role in osteolysis

查看全文 作　　者：Haemin [1]Kim;Bongjun [1]Kim;Sang Il [2,3,4]Kim;Hyung Joon [5]Kim;Brian [6]YRyu;Junho [2,3,7]Chung;Zang Hee [1]Lee;Hong-Hee [1]Kim

机构地区：[1]Department of Cell and Developmental Biology,BK21 Program and DRI,Seoul National University,Seoul,Korea;[2]Department of Biochemistry and Molecular Biology,Seoul National University College of Medicine,Seoul,Korea;[3]Cancer Research Institute,Seoul National University College of Medicine,Seoul,Korea;[4]Department of Cancer Biology,Seoul National University College of Medicine,Seoul,Korea;[5]Department of Oral Physiology,BK21 PLUS Project,and Dental and Life Science Institute,School of Dentistry,Pusan National University,Yangsan,Korea;[6]Interdisciplinary Program in Bioinformatics,Seoul National University College of Natural Sciences,Seoul,Korea;[7]Department of Biomedical Sciences,Seoul National University Graduate School,Seoul,Korea

出　　处：《Bone Research》索引2019年第7卷第4期,共13页

基　　金：supported by grants from the National Research Foundation of Korea (NRF2017R1A2A1A17069648 and NRF-2018R1A5A2024418) to H.-H.K.;the National Research Foundation of Korea (NRF-2017R1D1A1B03028003) to H.K. 摘　　要：Bone destruction induced by breast cancer metastasis causes severe complications,including death,in breast cancer patients.Communication between cancer cells and skeletal cells in metastatic bone microenvironments is a principal element that drives tumor progression and osteolysis.Tumor-derived factors play fundamental roles in this form of communication.To identify soluble factors released from cancer cells in bone metastasis,we established a highly bone-metastatic subline of MDA-MB-231 breast cancer cells.This subline(mtMDA)showed a markedly elevated ability to secrete S100A4 protein,which directly stimulated osteoclast formation via surface receptor RAGE.Recombinant S100A4 stimulated osteoclastogenesis in vitro and bone loss in vivo.Conditioned medium from mtMDA cells in which S100A4 was knocked down had a reduced ability to stimulate osteoclasts.Furthermore,the S100A4 knockdown cells elicited less bone destruction in mice than the control knockdown cells.In addition,administration of an anti-S100A4 monoclonal antibody(mAb)that we developed attenuated the stimulation of osteoclastogenesis and bone loss by mtMDA in mice.Taken together,our results suggest that S100A4 released from breast cancer cells is an important player in the osteolysis caused by breast cancer bone metastasis. 关键词：S100A4 breast METASTATIC

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S100A4 released from highly bone-metastatic breast cancer cells plays a critical role in osteolysis

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