Open AccessOverexpression of YB 1 C‐terminal domain inhibits proliferation, angiogenesis and tumorigenicity in a SK ‐ BR ‐3 breast cancer xenograft mouse model
Author(s) -
Shi Jianhong,
Cui Naipeng,
Wang Shuo,
Zhao Mingzhi,
Wang Bing,
Wang Yanan,
Chen Baoping
Publication year - 2016
Publication title -
febs open bio
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.718
H-Index - 31
ISSN - 2211-5463
DOI - 10.1002/2211-5463.12004
Subject(s) - angiogenesis , cell growth , cancer research , cell culture , ctd , biology , chemistry , microbiology and biotechnology , biochemistry , oceanography , genetics , geology
Y‐box‐binding protein 1 ( YB 1) 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 ( YB 1 CTD ) in proliferation, angiogenesis and tumorigenicity in breast cancer. Breast cancer cell line SK ‐ BR ‐3 was infected with GFP ‐tagged YB 1 CTD adenovirus expression vector. An 3‐(4,5‐dimethylthiazol‐2‐yl)‐5‐(3‐carboxymethoxyphenyl)‐2‐(4‐sulfophenyl)‐2H‐tetrazolium ( MTS ) proliferation assay showed that YB 1 CTD decreased SK ‐ BR ‐3 cell proliferation, and down‐regulated cyclin B1 and up‐regulated p21 levels in SK ‐ BR ‐3 cells. YB 1 CTD overexpression changed the cytoskeletal organization and slightly inhibited the migration of SK ‐ BR ‐3 cells. YB 1 CTD also inhibited secreted VEGF expression in SK ‐ BR ‐3 cells, which decreased SK ‐ BR ‐3‐induced EA .hy926 endothelial cell angiogenesis in vitro . YB 1 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 YB 1 CTD overexpression in inhibiting proliferation, angiogenesis and tumorigenicity of breast cancer cell line SK ‐ BR ‐3.