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The chromodomain helicase DNA binding protein 5 (CHD5) has recently been identified as a tumor suppressor in a mouse model. The  CHD5  locus at 1 p 36 is deleted, and its mutation has been detected in breast cancer. We, therefore, evaluated whether  CHD5  plays a role in human breast cancer.    Methods  We screened mutations in 55 tumors, determined promoter methylation in 39 tumors, measured RNA expression in 90 tumors, analyzed protein expression in 289 tumors, and correlated expression changes with clinicopathological characteristics of breast cancer. Functional effects of CHD5 on cell proliferation, invasion and tumorigenesis were also tested.    Results  Although only one mutation was detected,  CHD5  mRNA expression was significantly reduced, accompanied by frequent genomic deletion and promoter methylation, in breast cancer. The extent of methylation was significantly associated with reduced mRNA expression, and demethylating treatment restored  CHD5  expression. Lower  CHD5  mRNA levels correlated with lymph node metastasis ( P  = 0.026). CHD5 protein expression was also reduced in breast cancer, and lack of CHD5 expression significantly correlated with higher tumor stage, ER/PR-negativity, HER2 positivity, distant metastasis and worse patient survival ( P  ≤ 0.01). Functionally, ectopic expression of  CHD5  in breast cancer cells inhibited cell proliferation and invasion  in vitro  and tumorigenesis in nude mice. Consistent with the inhibition of invasion, CHD5 down-regulated mesenchymal markers vimentin, N-cadherin and ZEB1 in breast cancer cells.    Conclusion  Down-regulation of CHD5, mediated at least in part by promoter methylation, contributes to the development and progression of human breast cancer.

Chromodomain helicase DNA binding protein 5 plays a tumor suppressor role in human breast cancer