HDAC5 loss in pancreatic cancer induces enhanced arachidonic acid metabolism via overactivated GATA1-cPLA2 axis

Unlike class I Histone deacetylase (HDAC) members (HDAC1, 2, 3, etc.), HDAC5, a class IIa HDAC member, is downregulated in multiple solid tumors, including pancreatic cancer, and its loss is associated with unfavorable prognosis. Additionally, HDAC5’s expression correlates negatively with arachidonic acid (AA) metabolism, which is highly implicated in inflammatory responses and cancer progression. This study aimed to elucidate the role of HDAC5 in AA metabolism and its prospect in the treatment of pancreatic cancer. RNA-seq were applied in BxPC-3 cells. GATA1 ChIP-seq were applied in control and HDAC5 knock-down PANC-1 cells.