Send to

Choose Destination
FEBS Open Bio. 2016 Jan 11;6(1):33-42. doi: 10.1002/2211-5463.12004. eCollection 2016 Jan.

Overexpression of YB1 C-terminal domain inhibits proliferation, angiogenesis and tumorigenicity in a SK-BR-3 breast cancer xenograft mouse model.

Author information

Central Laboratory Hebei Laboratory of Mechanism and Procedure of Cancer Radiotherapy and Chemotherapy Affiliated Hospital of Hebei University Baoding China.
Department of Oncology Affiliated Hospital of Hebei University Baoding China.
Department of Pathology Affiliated Hospital of Hebei University Baoding China.


Y-box-binding protein 1 (YB1) is a multifunctional transcription factor with vital roles in proliferation, differentiation and apoptosis. In this study, we have examined the role of its C-terminal domain (YB1 CTD) in proliferation, angiogenesis and tumorigenicity in breast cancer. Breast cancer cell line SK-BR-3 was infected with GFP-tagged YB1 CTD adenovirus expression vector. An 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) proliferation assay showed that YB1 CTD decreased SK-BR-3 cell proliferation, and down-regulated cyclin B1 and up-regulated p21 levels in SK-BR-3 cells. YB1 CTD overexpression changed the cytoskeletal organization and slightly inhibited the migration of SK-BR-3 cells. YB1 CTD also inhibited secreted VEGF expression in SK-BR-3 cells, which decreased SK-BR-3-induced EA.hy926 endothelial cell angiogenesis in vitro. YB1 CTD overexpression attenuated the ability of SK-BR-3 cells to form tumours in nude mice, and decreased in vivo VEGF levels and angiogenesis in the xenografts in SK-BR-3 tumour-bearing mice. Taken together, our findings demonstrate the vital role of YB1 CTD overexpression in inhibiting proliferation, angiogenesis and tumorigenicity of breast cancer cell line SK-BR-3.


C‐terminal domain; SK‐BR‐3; Y‐box‐binding protein 1; angiogenesis; breast cancer; proliferation

Supplemental Content

Full text links

Icon for Wiley Icon for PubMed Central
Loading ...
Support Center