MP29-01: DNA replication stress by the loss of male ... lase ‘KDM5D’ in aggressive prostate cancer (APL - 2018)

DNA replication stress by the loss of male specific histone demethylase ‘KDM5D’ in aggressive prostate cancer

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INTRODUCTION

We previously demonstrated that loss of male specific histone demethylase &[prime]KDM5D&[prime] is associated with docetaxel resistance (Komura et al, 2016, PNAS). Decreased KDM5D expression seemed to be attributed to the deletion of copy number loss at Yq11 in prostate cancer.

METHODS

RNAseq and ChIPseq were performed to elucidate the biological function of KDM5D using hormone sensitive LNCaP cells (KDM5D positive) and corresponding LNCaP-104R2 CRPC cells (KDM5D negative by copy number loss of Y chromosome). Clinical impact of the genes regulated by KDM5D were further examined in TCGA and Health Professionals Follow-Up Study (PHS/HPFS) cohorts.

RESULTS

Gene Set Enrichment Analysis (GSEA) from the data of RNAseq in LNCaP (control vs sh-KDM5D#1 and #3) and LNCaP-104R2 (control vs KDM5D overexpression) revealed 64 positively enriched and 101 negatively enriched pathways with a false discovery rate (FDR)