谷氨酸羧肽酶Ⅱ
前列腺癌
膜
前列腺
抗原
阉割
癌症研究
医学
癌症
化学
内科学
免疫学
激素
生物化学
作者
Yu Li,Hongji Li,Keying Zhang,Xu Chao,Jingwei Wang,Zeyu Li,Yike Zhou,Бо Лю,Xiaolong Zhao,Zhengxuan Li,Jing Wang,Wei Hu,Yuming Jing,Peng Wu,Jingliang Zhang,Changhong Shi,Rui Zhang,Wenkai Jiang,Nianzeng Xing,Weihong Wen,Donghui Han,Weijun Qin
标识
DOI:10.1002/advs.202401095
摘要
Conventional androgen deprivation therapy (ADT) targets the androgen receptor (AR) inhibiting prostate cancer (PCa) progression; however, it can eventually lead to recurrence as castration-resistant PCa (CRPC), which has high mortality rates and lacks effective treatment modalities. The study confirms the presence of high glutathione peroxidase 4 (GPX4) expression, a key regulator of ferroptosis (i.e., iron-dependent program cell death) in CRPC cells. Therefore, inducing ferroptosis in CRPC cells might be an effective therapeutic modality for CRPC. However, nonspecific uptake of ferroptosis inducers can result in undesirable cytotoxicity in major organs. Thus, to precisely induce ferroptosis in CRPC cells, a genetic engineering strategy is proposed to embed a prostate-specific membrane antigen (PSMA)-targeting antibody fragment (gy1) in the macrophage membrane, which is then coated onto mesoporous polydopamine (MPDA) nanoparticles to produce a biomimetic nanoplatform. The results indicate that the membrane-coated nanoparticles (MNPs) exhibit high specificity and affinity toward CRPC cells. On further encapsulation with the ferroptosis inducers RSL3 and iron ions, MPDA/Fe/RSL3@M-gy1 demonstrates superior synergistic effects in highly targeted ferroptosis therapy eliciting significant therapeutic efficacy against CRPC tumor growth and bone metastasis without increased cytotoxicity. In conclusion, a new therapeutic strategy is reported for the PSMA-specific, CRPC-targeting platform for ferroptosis induction with increased efficacy and safety.
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