Cyclin-D1 And MUC1 Mediated Control Of Breast Cancer Cell Quiescence

Abstract

The overexpression of cyclin-D1 has been shown previously to be a factor in regulating a shallow state of quiescence in breast cancer cells. This is thought to be due to the increased trafficking of EGFR, a cyclin-D1 transcription cofactor, to the nucleus as a result of interaction with MUC1.¹’² This study sought to create an accurate in vitro model of quiescent behavior and its regulation mechanism that can then be manipulated to find ways to modulate quiescence. In collaboration with Léa Boden, a model was identified for MDA-MB-468 triple negative breast cancer cells³. In MDA-MB-468 cells, shMUC1 variants had lower levels of cyclin-D1 expression and lower levels of chromatin-bound EGFR than the shCTL variants, thus supporting that MUC1 interaction affects EGFR trafficking to the nucleus.