Silencing of Mad2 and BubR1 in MKN45 and ST2957 cells decreased their cell proliferation, migration and invasion abilities, indicating that Mad2 and BubR1 could contribute to cellular transformation and tumor progression in GC.
High-level MAD2 expression was observed in 26.3% (94 of 358 cases), and correlated with male sex (P=0.0002), tumor progression (pT status) (P=0.0009), visceral or parietal pleural invasion (P=0.0151), non-adenocarcinoma, histological classification (P<0.0001), and smoking history (P=0.0022), but not with patient age or lymph node metastasis (pN status).
Here, we show that CIN in cultured cells lacking Rb family proteins requires Mad2 upregulation and that this upregulation is also necessary for CIN and tumor progression in vivo.
Both over and under expression of the MAD2 and BUB1 mitotic spindle checkpoint genes were detected at all Barrett's histological stages with no apparent selective trend with neoplastic progression.