Targeting Histone Abnormality in Triple Negative Breast Cancer
Abstract
In this funding period, we continued to test the hypothesis that silencing of key tumor suppressive genes by enhanced crosstalk between LSD1 and HDAC5 is a unique epigenetic mechanism promoting TNBC growth, and blockade of the HDAC5-LSD1 axis results in profound inhibition of TNBC growth and metastasis. By using In vitro pull-down assays with His-tag recombinant LSD1 protein incubating withHDAC5 full-length or deletion mutants and immunofluorescence assays, we identified that HDAC5 domain containing nuclear localization element is essential for interaction with LSD1.
Document Details
- Document Type
- Technical Report
- Publication Date
- Aug 01, 2016
- Accession Number
- AD1024764
Entities
People
- Yi Huang
Organizations
- University of Pittsburgh