Tumor suppressor SET9 guides the epigenetic plasticity of breast cancer cells and serves as an early-stage biomarker for predicting metastasis
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- (rev. 4)
- Hyungyong Kim
- Date Published
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.
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Table of Contents
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 #
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