Ovarian cancer (OC) is a common malignant cancer in women with a low overall survival rate, and ferroptosis may be a potential new strategy for treatment. Six-transmembrane epithelial antigen of prostate 3 (STEAP3) is a gene closely related to ferroptosis, yet the role of STEAP3 in OC has not yet been thoroughly investigated. Using biological information analysis, we first found that STEAP3 was highly expressed in OC, which was significantly associated with poor prognosis of patients and was an independent prognostic factor. Through cloning, scratch, and transwell experiments, we subsequently found that knockdown of STEAP3 significantly reduced the proliferation and migration ability of OC cells. Furthermore, we found that knockdown of STEAP3 induced ferroptosis in OC cells by detecting ferroptosis indicators. Mechanistically, we also found that knockdown of STEAP3 induced ferroptosis through the p53/SLC7A11 signaling pathway. Through tumorigenic experiments in nude mice, we finally verified that the knockdown of STEAP3 could inhibit tumor growth in vivo by promoting ferroptosis through the p53 pathway. Overall, our study identified a novel therapeutic target for ferroptosis in OC and explored its specific mechanism of action.

中文翻译：

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STEAP3 通过 p53/SLC7A11 途径调节铁死亡，影响卵巢癌进展

卵巢癌（OC）是女性常见的恶性肿瘤，总体生存率较低，铁死亡可能是一种潜在的新治疗策略。前列腺六跨膜上皮抗原3（STEAP3）是与铁死亡密切相关的基因，但STEAP3在OC中的作用尚未得到深入研究。通过生物学信息分析，我们首先发现STEAP3在OC中高表达，其与患者不良预后显着相关，是独立的预后因素。通过克隆、划痕和transwell实验，我们随后发现STEAP3的敲低显着降低了OC细胞的增殖和迁移能力。此外，我们通过检测铁死亡指标发现 STEAP3 的敲低会诱导 OC 细胞铁死亡。从机制上讲，我们还发现 STEAP3 的敲低通过 p53/SLC7A11 信号通路诱导铁死亡。通过裸鼠致瘤实验，我们最终验证了STEAP3的敲低可以通过p53途径促进铁死亡来抑制体内肿瘤生长。总体而言，我们的研究确定了 OC 铁死亡的新治疗靶点，并探讨了其具体作用机制。