PTRF/Cavin-1 对癌细胞铁突变的调控。

IF 3.6 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Free Radical Research Pub Date : 2024-05-01 Epub Date: 2024-08-07 DOI:10.1080/10715762.2024.2386457
Hui Xiang, Miao Wang, Yi-Fang Chen, Hao-Ming Wu, Ming-Ge Li, Lei Guo, Ying-Yi Zhang, He-Zhe Lu
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引用次数: 0

摘要

卵巢癌复发率高,因此需要新的治疗策略来改善患者的预后。诱导卵巢癌细胞的铁蜕变是潜在的策略之一。铁变性是一种主要发生在细胞膜上的铁依赖型、脂质过氧化驱动的细胞死亡模式。PTRF是位于细胞膜上的洞穴结构的一个组成部分,参与多种生理过程,包括但不限于内吞、信号转导和脂质代谢。本研究阐明了卵巢癌中 PTRF 与铁突变之间的关系,为开发新的治疗策略提供了新的视角。我们用 siRNA 敲除了卵巢癌细胞株 HEY 和 SKOV3 中的 PTRF,然后用 Erastin(Era)刺激铁突变。我们的研究表明,缺乏 PTRF 会使癌细胞对铁凋亡敏感,可能是通过改变膜的稳定性和张力,从而影响与铁凋亡相关的信号通路,如脂质和动脉粥样硬化、流体剪切应力和动脉粥样硬化。我们的发现为开发卵巢癌的新疗法提供了新的见解。
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Regulation of cancer cell ferroptosis by PTRF/Cavin-1.

Ovarian cancer, marked by high rate of recurrence, novel therapeutic strategies are needed to improve patient outcome. One of the potential strategies is inducing ferroptosis in ovarian cancer cells. Ferroptosis is an iron-dependent, lipid peroxidation-driven mode of cell death primarily occurring on the cell membrane. PTRF, an integral component of the caveolae structures located on the cell membrane, is involved in a multitude of physiological processes, including but not limited to, endocytosis, signal transduction, and lipid metabolism. This study elucidates the relationship between PTRF and ferroptosis in ovarian cancer, offering a fresh perspective for the development of new therapeutic strategies. We knocked down PTRF employing siRNA in the ovarian cancer cell lines HEY and SKOV3, following which we stimulated ferroptosis with Erastin (Era). Our research indicates that the lack of PTRF sensitizes cancer cells to ferroptosis, likely by altering membrane stability and tension, thereby affecting signal pathways related to ferroptosis, such as lipid and atherosclerosis, fluid shear stress, and atherosclerosis. Our findings provide new insights for developing new treatments for ovarian cancer.

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来源期刊
Free Radical Research
Free Radical Research 生物-生化与分子生物学
CiteScore
6.70
自引率
0.00%
发文量
47
审稿时长
3 months
期刊介绍: Free Radical Research publishes high-quality research papers, hypotheses and reviews in free radicals and other reactive species in biological, clinical, environmental and other systems; redox signalling; antioxidants, including diet-derived antioxidants and other relevant aspects of human nutrition; and oxidative damage, mechanisms and measurement.
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