铁死亡被认为是非凋亡性程序性细胞死亡，被认为是一种新的抗肿瘤治疗策略。短转录诱导物-1 (FBI-1) 结合因子是一种重要的原癌基因，在人类恶性肿瘤和治疗耐药性的发展中发挥多种作用。然而，FBI-1在内分泌非依赖性前列腺癌铁死亡中的作用仍不清楚。本研究结果表明，FBI-1通过miR-324-3p/谷胱甘肽过氧化物酶4（miR-324-3p/GPX4）抑制前列腺癌PC-3细胞（典型的内分泌非依赖性前列腺癌细胞系）的铁死亡。 ）轴。 FBI-1 的过表达增强了 GPX4 的表达水平。相反，敲除FBI-1会降低GPX4的表达并诱导PC-3细胞的铁死亡。 miR-324-3p 通过靶向 GPX4 的 3'-非翻译区来诱导铁死亡，从而降低 GPX4 的表达。值得注意的是，FBI-1 通过抑制 miR-324-3p 的水平来增加 GPX4 的表达。 miR-324-3p 的转录由特异性蛋白 1 (SP1) 介导，FBI-1 通过抑制 SP1 的激活来抑制 miR-324-3p 的表达。在临床标本中，FBI-1的内源水平与谷胱甘肽过氧化物酶4（GPX4）呈正相关，与miR-324-3p的表达呈负相关。因此，结果表明miR-324-3p/GPX4轴参与FBI-1介导的前列腺癌细胞铁死亡。©作者。

Ferroptosis has been characterized as non-apoptotic programmed cell death and is considered a novel strategy for antitumor treatment. The factor that binds to inducer of short transcripts-1 (FBI-1) is an important proto-oncogene playing multiple roles in human malignancies and the development of resistance to therapy. However, the roles of FBI-1 in ferroptosis of endocrine independent prostate carcinoma are still unknown. The results of this study showed that FBI-1 inhibited the ferroptosis of prostate carcinoma PC-3 cells (a typical endocrine-independent prostate carcinoma cell line) via the miR-324-3p/glutathione peroxidase 4 (miR-324-3p/GPX4) axis. Overexpression of FBI-1 enhanced the expression levels of GPX4. In contrast, knockdown of FBI-1 decreased the expression of GPX4 and induced the ferroptosis of PC-3 cells. The miR-324-3p decreased the expression of GPX4 by targeting the 3'-untranslated region of GPX4 to induce ferroptosis. Notably, FBI-1 increased the expression of GPX4 by repressing the levels of miR-324-3p. The transcription of miR-324-3p was mediated by specificity protein 1 (SP1), and FBI-1 repressed the expression of miR-324-3p by repressing the activation of SP1. In clinical specimens, the endogenous levels of FBI-1 were positively associated with Glutathione Peroxidase 4 (GPX4) and negatively related with the expression of miR-324-3p. Therefore, the results indicated that the miR-324-3p/GPX4 axis participates in the FBI-1-mediated ferroptosis of prostate carcinoma cells.© The author(s).