Title MAGE-D1 inhibits proliferation, migration and invasion of human breast cancer cells
Authors Du, Qiang
Zhang, Yang
Tian, Xin-Xia
Li, Yan
Fang, Wei-Gang
Affiliation Peking Univ, Hlth Sci Ctr, Dept Pathol, Key Lab Carcinogenesis & Translat Res,Minist Educ, Beijing 100191, Peoples R China.
Keywords breast cancer
MAGE-D1
invasion
P75 NEUROTROPHIN RECEPTOR
INTERACTING PROTEIN
FAMILY PROTEIN
IN-VITRO
NRAGE
APOPTOSIS
DLXIN-1
DEATH
BRCA2
GENE
Issue Date 2009
Publisher oncology reports
Citation ONCOLOGY REPORTS.2009,22,(3),659-665.
Abstract MAGE-D1, also known as NRAGE or Dixin-1, is a member of the MAGE family of proteins. It interacts with multiple adaptors and mediates various cellular functions such as regulation of apoptosis, transcription, cell cycle, cell adhesion and angiogenesis. In this study, we evaluated the effect of MAGE-D1 plasmid transfection on the growth, migration and invasion of breast cancer cells. MTT assay and cell counting consistently showed that MAGE-D1 transfection could effectively inhibit the proliferation of breast cancer cells. However, further FACS analyses failed to demonstrate any alterations in cell cycle distribution and apoptosis after MAGE-D1 transfection. In vitro scratch wound healing assay exhibited that MAGE-D I suppressed cell migration. In addition, Boyden chamber invasion assay showed that MAGE-D1 significantly inhibited cell invasion. Furthermore, in an attempt to elucidate the mechanism of MAGE-D1 in suppressing cellular growth and invasion, the protein expressions of p53, p21, E-cadherin, beta-catenin, MMP-2 and MMP-9 were assessed. Western blotting showed that MAGE-D1 upregulated the expression of p53, p21 and E-cadherin, whereas down-regulated beta-catenin expression. Taken together, this study suggests that MAGE-D1 play important roles in the regulation of cell proliferation, migration and invasion of breast cancer cells. Enhanced expression of MAGE-D I by gene transfer could reverse the malignant phenotypes of breast cancer cells. MAGE-D1 may be a potential therapeutic target for breast cancer.
URI http://hdl.handle.net/20.500.11897/344850
ISSN 1021-335X
DOI 10.3892/or_00000486
Indexed SCI(E)
PubMed
Appears in Collections: 医学部待认领

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