Format

Send to

Choose Destination
See comment in PubMed Commons below
PLoS One. 2013 May 7;8(5):e62936. doi: 10.1371/journal.pone.0062936. Print 2013.

BSP gene silencing inhibits migration, invasion, and bone metastasis of MDA-MB-231BO human breast cancer cells.

Author information

1
Department of Medical Research, Guangzhou General Hospital of Guangzhou Military Command, Guangzhou, Guangdong Province, China. jiew@tom.com

Erratum in

  • PLoS One. 2014;9(1). doi:10.1371/annotation/d514b852-6b48-4720-a245-080daeb5eb05.

Abstract

Bone sialoprotein (BSP) has been implicated in a variety of physiological and pathophysiological events, including tumor cell invasion, bone homing, adhesion, and matrix degradation. To explore the potential involvement of BSP in human breast cancer cell invasion and metastasis, we used retrovirus-mediated RNAi to deplete BSP levels in the human bone-seeking breast cancer cell line MDA-MB-231BO (231BO) and established the 231BO-BSP27 and 231BO-BSP81 cell clones. Cell proliferation, colony formation, wound healing, and the ability to invade into matrigel of these BSP-depleted clones were all decreased. Both 231BO-BSP27 cells and 231BO-BSP81 cells showed a significant (15.4% and 28.6% respectively) reduction of bone metastatic potential following intracardiac injection as determined by X-ray detection and by hematoxylin and eosin staining. Moreover, the expression of integrins αvβ3 and β3 was decreased in the BSP-silenced cells whereas ectopic BSP expression increased the integrins αvβ3 and β3 levels. These results together suggest that BSP silencing decreased the integrin αvβ3 and β3 levels, in turn inhibiting cell migration and invasion and decreasing the ability of the cells to metastasize to bone.

PMID:
23667544
PMCID:
PMC3647072
DOI:
10.1371/journal.pone.0062936
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Public Library of Science Icon for PubMed Central
    Loading ...
    Support Center