From Mechanisms to Therapy: Exploring the Role of Ferroptosis in Cervical Cancer Transformation and Treatment.

IF 2.5 3区生物学 Q3 CELL BIOLOGY

Traffic Pub Date : 2025-07-01 DOI:10.1111/tra.70018

Zhenlei Wang, Yuanyuan Xiao, Ranzhong Chen, Erqun Tang, Shuangyang Tang

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引用次数: 0

Abstract

Cervical cancer (CC) exerts a considerable impact on women's health worldwide and presents persistent challenges to conventional therapeutic strategies due to its propensity for distant metastasis, postoperative recurrence, and variable drug resistance. Ferroptosis, a recently identified type of programmed cell death, offers promising potential for a therapeutic approach for CC. This paper reviews the regulatory processes involved in ferroptosis, including the sequential events leading to cell membrane rupture via lipid peroxidation and the changes in ferroptosis sensitivity as cervical cells progress from a healthy to a malignant condition. Additionally, the dynamic relationship between ferroptosis and CC transformation driven by high-risk HPV (HR-HPV) infection is examined, with a particular focus on how HR-HPV E6/E7 proteins influence ferroptosis sensitivity. By examining the factors associated with ferroptosis, this review provides insights into CC progression and prognosis. Furthermore, therapeutic strategies targeting ferroptosis are discussed, offering novel perspectives for effective treatment options for CC.

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从机制到治疗：探讨铁下垂在宫颈癌转化和治疗中的作用。

宫颈癌（CC）对全世界妇女的健康产生了相当大的影响，由于其远处转移、术后复发和可变耐药性的倾向，对传统的治疗策略提出了持续的挑战。铁下垂是最近发现的一种程序性细胞死亡类型，为CC的治疗提供了有希望的治疗方法。本文综述了铁下垂的调控过程，包括通过脂质过氧化导致细胞膜破裂的一系列事件，以及随着宫颈细胞从健康状态向恶性状态发展，铁下垂敏感性的变化。此外，研究了高危HPV （HR-HPV）感染驱动的铁下垂与CC转化之间的动态关系，特别关注HR-HPV E6/E7蛋白如何影响铁下垂敏感性。通过检查与铁下垂相关的因素，本综述提供了CC进展和预后的见解。此外，针对铁下垂的治疗策略进行了讨论，为CC的有效治疗选择提供了新的视角。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Traffic 生物-细胞生物学

CiteScore

8.10

自引率

2.20%

发文量

审稿时长

2 months

期刊介绍： Traffic encourages and facilitates the publication of papers in any field relating to intracellular transport in health and disease. Traffic papers span disciplines such as developmental biology, neuroscience, innate and adaptive immunity, epithelial cell biology, intracellular pathogens and host-pathogen interactions, among others using any eukaryotic model system. Areas of particular interest include protein, nucleic acid and lipid traffic, molecular motors, intracellular pathogens, intracellular proteolysis, nuclear import and export, cytokinesis and the cell cycle, the interface between signaling and trafficking or localization, protein translocation, the cell biology of adaptive an innate immunity, organelle biogenesis, metabolism, cell polarity and organization, and organelle movement. All aspects of the structural, molecular biology, biochemistry, genetics, morphology, intracellular signaling and relationship to hereditary or infectious diseases will be covered. Manuscripts must provide a clear conceptual or mechanistic advance. The editors will reject papers that require major changes, including addition of significant experimental data or other significant revision. Traffic will consider manuscripts of any length, but encourages authors to limit their papers to 16 typeset pages or less.