研究动态
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癌症中竞争性内源 RNA 网络和铁死亡:新的治疗靶点。

Competing endogenous RNA networks and ferroptosis in cancer: novel therapeutic targets.

发表日期:2024 May 22
作者: Fatemeh Nejadi Orang, Mahdi Abdoli Shadbad
来源: Cell Death & Disease

摘要:

作为一种新发现的受调节细胞死亡,铁死亡是一种依赖铁的代谢驱动过程,与多不饱和脂肪酰基过氧化、活性氧 (ROS) 水平升高和线粒体损伤有关。这种独特的受调节细胞死亡在各种癌症中都失调。激活恶性细胞中的铁死亡可增加不同恶性肿瘤的癌症免疫治疗和放化疗反应。在过去的十年中,不断积累的研究提供了非编码 RNA (ncRNA) 和竞争性内源 RNA (ceRNA) 网络之间串扰的证据,并强调了它们在恶性肿瘤发生和进展中的重要性。除了调节铁死亡的药物外,最近的研究还揭示了在癌症治疗中恢复失调的铁死亡相关 ceRNA 网络的潜力。本研究对铁死亡的意义、铁死亡途径、铁死亡在癌症免疫治疗和放化疗中的作用、ceRNA 生物发生以及不同癌症中铁死亡调节 ceRNA 网络进行了全面且最新的综述。所提供的见解可以为作者提供有关铁死亡和铁死亡相关 ceRNA 网络及其对治疗和确定受影响患者预后的影响的最新发现和未来前景。© 2024。作者。
As a newly identified regulated cell death, ferroptosis is a metabolically driven process that relies on iron and is associated with polyunsaturated fatty acyl peroxidation, elevated levels of reactive oxygen species (ROS), and mitochondrial damage. This distinct regulated cell death is dysregulated in various cancers; activating ferroptosis in malignant cells increases cancer immunotherapy and chemoradiotherapy responses across different malignancies. Over the last decade, accumulating research has provided evidence of cross-talk between non-coding RNAs (ncRNAs) and competing endogenous RNA (ceRNA) networks and highlighted their significance in developing and progressing malignancies. Aside from pharmaceutical agents to regulate ferroptosis, recent studies have shed light on the potential of restoring dysregulated ferroptosis-related ceRNA networks in cancer treatment. The present study provides a comprehensive and up-to-date review of the ferroptosis significance, ferroptosis pathways, the role of ferroptosis in cancer immunotherapy and chemoradiotherapy, ceRNA biogenesis, and ferroptosis-regulating ceRNA networks in different cancers. The provided insights can offer the authorship with state-of-the-art findings and future perspectives regarding the ferroptosis and ferroptosis-related ceRNA networks and their implication in the treatment and determining the prognosis of affected patients.© 2024. The Author(s).