Chromatin state upon MSK1 downregulation by shRNA in dormant bone metastatic (DBM) cells.

For many breast cancer (BCa) patients, symptomatic bone metastases appear after years or even decades of latency. How metastatic cells disseminate, and how micromet­astatic lesions remain dormant and undetectable, are major questions in cancer research. Here we identify and func­tionally analyse a molecular mechanism involved in the bone metastatic latency of estrogen receptor (ER)+ BCa. Overall design: ChIP-sequencing was performed on DBM shCTRL and DBM shMSK1 cells using antibodies recognizing 4 chromatin marks at histone H3 (H3K9ac, H3K9me3, H3K27ac, H3K27me3).