Cytosolic Phospholipase A2 Determines Intercellular Heterogeneity of Stress Granules and Chemotherapy Response

Because of their defective G1 checkpoint mechanisms, cancer cells often activate a G2 checkpoint, which leads to resistance to DNA-damaging chemotherapeutics. We identify an intercellular heterogeneity of SGs that is driven by the cell cycle, with SG formation being highest in the G2 phase. Targeting G2-specific SG formation sensitizes pancreatic tumors to G2 arrest-inducing chemotherapeutics.