Ray Suman Kumar, Mukherjee Sukhes
Independent researcher, Bhopal, Madhya Pradesh, 462020, India.
Department of Biochemistry, All India Institute of Medical Sciences, Bhopal, Madhya Pradesh, 462020, India.
Curr Mol Med. 2024;24(12):1470-1482. doi: 10.2174/1566524023666230913105735.
Ferroptosis is a nonapoptotic, iron-dependent form of cell death that can be actuated in disease cells by expected improvements and manufactured specialists. Different studies have recently resurrected the role of this newly discovered cell death pathway and demonstrated its efficacy in treating breast cancer. Breast cancer is the most well-known type of cancer among women worldwide. Despite many years of research focusing on cell death in breast cancer, counting apoptosis, clinical treatment leftovers are difficult due to the high likelihood of recurrence. Ferroptosis is defined by a lack of lipid peroxide repair capacity by phospholipid hydroperoxides GPX4, accessibility of redox-active iron, and followed oxidation of polyunsaturated fatty acids acid-containing phospholipids signalling, amino acid and iron metabolism, ferritinophagy, epithelial-tomesenchymal transition, cell adhesion, and mevalonate and phospholipid biosynthesis can all be factors that influence ferroptosis susceptibility. Ferroptosis, an iron-dependent controlled cell death caused by excessive lipid peroxidation, has been entwined in breast cancer development and therapeutic response for the past decade. Advances in enhancing clinical drugs targeting ferroptosis are developing silver linings to treat breast cancer. Ferroptosis is influenced by metabolism and the expression of certain genes, making it a prospective therapeutic target for monitoring malignant growth and an appealing target for precision cancer medication disclosure. In the coming years, research into biomarkers to follow ferroptosis in patients with breast cancer and the course of events and the subsequent use of novel ferroptosis-based treatments will be captious. We present a fundamental analysis of the actual understanding of molecular mechanisms along with regulatory networks associated with ferroptosis, expected physiological functions in growth concealment, ferroptosis-associated differentially expressed genes, treatment targeting potential, and recent advances in the development of therapeutic strategies in this review.
铁死亡是一种非凋亡性、铁依赖性的细胞死亡形式，可由预期的刺激因素和化学合成物质在病变细胞中引发。最近的不同研究重新揭示了这种新发现的细胞死亡途径的作用，并证明了其在治疗乳腺癌方面的有效性。乳腺癌是全球女性中最常见的癌症类型。尽管多年来对乳腺癌细胞死亡进行了诸多研究，包括细胞凋亡，但由于复发可能性高，临床治疗仍面临困难。铁死亡的定义是磷脂氢过氧化物谷胱甘肽过氧化物酶4（GPX4）缺乏修复脂质过氧化物的能力、氧化还原活性铁的存在，以及随后含多不饱和脂肪酸的磷脂信号转导、氨基酸和铁代谢、铁自噬、上皮-间质转化、细胞黏附以及甲羟戊酸和磷脂生物合成等过程的氧化，所有这些都可能是影响铁死亡易感性的因素。在过去十年中，铁死亡这种由过度脂质过氧化引起的铁依赖性可控细胞死亡，已与乳腺癌的发展和治疗反应紧密相连。增强针对铁死亡的临床药物的研究进展为治疗乳腺癌带来了希望。铁死亡受代谢和某些基因表达的影响，使其成为监测恶性肿瘤生长的潜在治疗靶点以及精准癌症药物研发的一个有吸引力的靶点。在未来几年，对乳腺癌患者铁死亡生物标志物及其进程的研究以及随后基于铁死亡的新型治疗方法的应用将至关重要。在本综述中，我们对铁死亡相关分子机制及调控网络的实际认识、在肿瘤抑制中的预期生理功能、铁死亡相关差异表达基因、治疗靶向潜力以及治疗策略开发的最新进展进行了基础分析。
