The spindle checkpoint protein MAD1 regulates the expression of E-cadherin             and prevents cell migration.
Aneuploidy is a common characteristic of human solid tumors. It has been             proposed that a defect of the spindle assembly checkpoint (SAC) generates aneuploidy             and might facilitate tumorigenesis. However, a direct link between the SAC proteins             and tumorigenesis has not yet been elucidated. Here, we demonstrate the association             of the SAC protein MAD1 with the RNA polymerase II complex and its role in gene             expression. Furthermore, MAD1 binds to the E-cadherin promoter region. Knockdown             of endogenous MAD1 by siRNA reduces E-cadherin expression and enhances the migration             ability of non-metastatic breast cancer cells, indicating that reduced MAD1 expression             is a new potential diagnostic symptom of tumor metastasis.
Institute of Medical Sciences, Department of Microbiology, Tzu-Chi University, Hualien 970, Taiwan, ROC.
Yvan
Y
Chen
Pei-Chi
PC
Yeh
Jing-Chun
JC
Huang
Chang-Ching
CC
Yeh
Yue-Li
YL
Juang
D015820:Cadherins / Q000235:genetics / Q000378:metabolism*; D018797:Cell Cycle Proteins / Q000235:genetics / Q000378:metabolism*; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000235:genetics; D015870:Gene Expression; D015972:Gene Expression Regulation, Neoplastic; D006367:HeLa Cells; D006801:Humans; D009687:Nuclear Proteins / Q000235:genetics / Q000378:metabolism*; D011485:Protein Binding; D021381:Protein Transport; D012319:RNA Polymerase II / Q000378:metabolism; D034741:RNA, Small Interfering / Q000235:genetics / Q000378:metabolism
D015820:Cadherins; D018797:Cell Cycle Proteins; C501384:MAD1L1 protein, human; D009687:Nuclear Proteins; D034741:RNA, Small Interfering; D012319:RNA Polymerase II