This could mean that increased nuclear export (of, for instance, pRb, p53, p73, BRCA1, p21, p27, E2F4, IκB, survivin), rather than spindle defects, mainly drives CIN and tumorigenesis.
E2F-4 is a member of the E2F family, located at chromosome band 16q22.1, that shows frequent deletion in breast cancer, suggesting that it may function as a TSG in breast carcinogenesis.
The frequency of the E2F-4 mutation in HNPCC was comparable with that in sporadic CRC with MSI-H. E2F-4 was considered to be one of the important target genes responsible for the carcinogenesis of HNPCC.
Our data suggest that a direct involvement of E2F4 in tumorigenesis is unlikely, although increased E2F4 expression may be associated with human cancer.
We report here a new cellular function of p27 as a transcriptional regulator in association with p130/E2F4 complexes that could be relevant for tumorigenesis.
The results of the present study demonstrated that E2F4 methylation status can have a notable influence on its expression, and that it may have prognostic value in breast carcinogenesis.