Epigenetics 조절에 의해 암세포의 multiple phenotypic states, 유연성(plasticity)이 가능해진다. SET9이 DNA methyltransferases-1 단백질의 안정성을 조절하여 SET9의 전사활성을 Snail과 함께 억제한다.

유방암에서의 SET9 발현 조절은 E2F1과 silencing of SET9의 연결이 EMT와 CSC을 유도한다.

SET9의 활성은 재발환자보다 complete remission 환자에게 더 높다. 따라서 Tumor suppressor gene이며, 예후 인자로 활용할 수 있다.

2016-05-14 김미정 저널 발표

Summary #

Introduction #

Results #

A negative feedback loop between SET9 and DNMT1 determines the epigenetic phenotype of BC cells #

SET9 contributes to the epigenetic regulation of epithelial– mesenchymal transition #

Snail cooperates with DNMT1 to repress SET9 expression #

SET9 and E2F1 are reciprocally regulated in BC cells #

Loss of SET9 activity acts as a molecular link between EMT and the generation of cells with stem cell-like properties #

SET9 as an early prognostic marker for BC malignancy #

Discussion #

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