Overexpression of CD9 in Human Breast Cancer Cells Promotes the Development of Bone Metastases

Bone is a preferred target for circulating metastatic breast cancer cells. We found that the CD9 protein was up-regulated in the B02 osteotropic cell line, derived from the aggressive parental MDA-MB-231 breast cancer cell line. Here, we investigated the putative relationship between CD9 expression...

Full description

Saved in:
Bibliographic Details
Published inAnticancer research Vol. 32; no. 12; pp. 5211 - 5220
Main Authors KISCHEL, Philippe, BELLAHCENE, Akeila, DEUX, Blandine, LAMOUR, Virginie, DOBSON, Rowan, DE PAUW, Edwin, CLEZARDIN, Philippe, CASTRONOVO, Vincent
Format Journal Article Web Resource
LanguageEnglish
Published Attiki International Institute of Anticancer Research 01.12.2012
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Bone is a preferred target for circulating metastatic breast cancer cells. We found that the CD9 protein was up-regulated in the B02 osteotropic cell line, derived from the aggressive parental MDA-MB-231 breast cancer cell line. Here, we investigated the putative relationship between CD9 expression and the osteotropic phenotype. Overexpression of CD9 was analyzed by immunoblotting in different cell lines. Immunohistochemistry was used to assess CD9 expression in primary tumors and metastatic lesions. In vivo experiments were conducted in mice using a monoclonal antibody against CD9. CD9 overexpression was confirmed in osteotropic cells. CD9 was significantly overexpressed in bone metastases versus primary tumors and visceral metastatic lesions. Finally, in vivo experiments showed that an antibody against CD9 delays homing of B02 cells in bone marrow, slowing down bone destruction. Our study reveals a potential implication of CD9 in the formation of bony metastases from breast cancer cells.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ObjectType-Article-2
ObjectType-Feature-1
info:eu-repo/grantAgreement/EC/FP7/201342
scopus-id:2-s2.0-84872589533
ISSN:0250-7005
1791-7530
1791-7530