DDP基于化疗的耐药是卵巢癌治疗失败的重要原因。不过，对化疗产生耐药的肿瘤细胞可能会暴露于其他细胞死亡途径的脆弱性下。在这里，我们发现DDP耐药性的卵巢癌细胞更容易受到Erastin引发的铁死亡诱导物的攻击。应该注意的是，这种脆弱性并不依赖于经典的铁死亡防御蛋白的减弱，而是由于铁蛋白重链（FTH1）的减少所引起的。DDP耐药性的卵巢癌细胞通过保持高水平的自噬来逃避化疗的压力，最终导致FTH1的自噬降解增加。我们进一步发现，AKT1的丧失是导致DDP耐药性卵巢癌细胞自噬水平增加的原因。我们的研究为通过针对铁死亡途径逆转DDP耐药性提供了新的见解，而AKT1可能是铁死亡易感性的分子标记。

Resistance to cisplatin (DDP) based chemotherapy is an important reason for the failure of ovarian cancer treatment. However, tumor cells resistant to chemotherapy may expose vulnerability to other cell death pathways. Here, we found that DDP resistant ovarian cancer cells are more susceptible to Erastin induced ferroptosis. It should be noted that this vulnerability does not depend on the weakening of classical ferroptosis defense proteins, but is caused by the reduction of ferritin heavy chain (FTH1). DDP resistant ovarian cancer cells maintain a high level of autophagy to escape the pressure of chemotherapy, which ultimately leads to increased autophagic degradation of FTH1. We further revealed that the loss of AKT1 was the reason for the increased autophagy level of DDP resistant ovarian cancer cells. Our study provides new insights into reversing DDP resistance in ovarian cancer by targeting ferroptosis pathway, and AKT1 may be a molecular marker of susceptibility to ferroptosis.