In the present study, we investigated the role of UHRF1 (
ubiquitin-like protein containing PHD and RING finger domains 1) in proliferation, invasion and migration of
breast cancer cells, and the potential mechanisms were also explored. Cell proliferation was examined by
3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay; cell cycle distribution and apoptosis were evaluated using flow cytometry;
protein expression was determined by western blotting; angiogenesis of xenografts was assessed by microvessel density (MVD); cell invasion was measured using transwell chamber; cell migration was determined by
wound scratching assay. Our results demonstrated that UHRF1 transfection conferred serum independence to MDA-MB-231 cells, G1 phase shortage and apoptosis suppression, accompanied with an increased expression of
cyclin D1 and decreased expression of Bax. Significant pro-invasion and pro-migration activity was observed, with no obvious effect on the expression of PTEN and
maspin. Co-expression of the UHRF1/PTEN or UHRF1/
maspin degraded the role of UHRF1 in regulating invasion and migration. UHRF1 induced growth of MDA-MB-231 cells by promoting
tumor vessel formation in vivo. In conclusion, UHRF1 promoted the proliferation of
breast cancer cells by apoptosis inhibition, G1 phase shortage and promotion of
tumor vessel formation, and pro-invasion and pro-migration activity was also observed by interacting with PTEN and
maspin. Thus, UHRF1 may serve as a new
therapy target for
breast cancer.