HIF1A and posterior cortical atrophy: Notably, iron also serves as co-factor for prolyl hydroxylase [34], and CCA-treated PCa cells under normoxic conditions display decreased HIF-1α hydroxylation and turnover (Figure 5C, and 5F) and increased HIF-1α translocation to the nucleus (Figure 4C); these effects are reversible following iron repletion (Figure 5C and 5F).