Abstract:
:Oncogenic activation of MYC occurs often in breast carcinoma and is associated with poor prognosis. Loss or inactivation of mechanisms that restrain MYC may therefore be involved in tumor progression. In this study, we show that the MYC-interacting adaptor protein BIN1 is frequently missing in malignant breast cells and that this loss is functionally significant. BIN1 was expressed in normal and benign cells and tissues but was undetectable in 6/6 estrogen receptor-positive or estrogen receptor-negative carcinoma cell lines examined. Similarly, complete or partial losses of BIN1 were documented in 30/50 (60%) cases of malignant breast tissue analyzed by immuno-histochemistry or RT-PCR. Abnormalities in the organization of the BIN1 gene were apparent in only a minority of these cases, suggesting that most losses were due to epigenetic causes. Nevertheless, they were functionally significant because ectopic BIN1 induced programmed cell death in malignant cells lacking endogenous BIN1 but had no effect on the viability of benign cells. We propose that loss of BIN1 may contribute to breast cancer progression by eliminating a mechanism that restrains the ability of activated MYC to drive cell division inappropriately.
journal_name
Int J Cancerjournal_title
International journal of cancerauthors
Ge K,Duhadaway J,Sakamuro D,Wechsler-Reya R,Reynolds C,Prendergast GCkeywords:
subject
Has Abstractpub_date
2000-02-01 00:00:00pages
376-83issue
3eissn
0020-7136issn
1097-0215pii
10.1002/(SICI)1097-0215(20000201)85:3<376::AID-IJCjournal_volume
85pub_type
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