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<p>Iron regulatory protein (IRP2) plays a key role in regulating iron metabolism and enables cell survival by activating mitochondrial function. Targeting IRP2 to disrupt iron homeostasis is a promising strategy for enhancing the efficacy of cancer treatments. Depletion of IRP2 in breast cancer (BC) cells is associated with sensitivity to radiation therapy (RT), and inhibition of IRP2 prior to RT significantly reduces cell viability compared with radiation treatment alone. This combined therapeutic effects of IRP2 inhibition and radiation treatment were observed in parental and radioresistant cancer cells, significantly enhancing the proportion of cell death. In conclusion, this study proposes that the genetic or pharmacological inhibition of IRP2 in BC cells may serve as a novel therapeutic strategy for increasing radiosensitivity and overcoming resistance by inducing mitochondrial dysfunction.</p>

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Targeting iron regulatory protein 2 (IRP2) to disrupt iron metabolism enhances radiosensitivity through mitochondrial dysfunction in breast cancer cells

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月31日

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  • Ye Yeong Jeong,
  • Jieon Hwang,
  • Areum Park,
  • Sungmin Cho,
  • Inyoung Cho,
  • Soseul Won,
  • You Me Shin,
  • Sung Eun Kim,
  • Chan Hoon Maeng,
  • Jaemoon Yang,
  • Minhee Ku,
  • Hyuk Lee,
  • Sang Joon Shin

摘要

Iron regulatory protein (IRP2) plays a key role in regulating iron metabolism and enables cell survival by activating mitochondrial function. Targeting IRP2 to disrupt iron homeostasis is a promising strategy for enhancing the efficacy of cancer treatments. Depletion of IRP2 in breast cancer (BC) cells is associated with sensitivity to radiation therapy (RT), and inhibition of IRP2 prior to RT significantly reduces cell viability compared with radiation treatment alone. This combined therapeutic effects of IRP2 inhibition and radiation treatment were observed in parental and radioresistant cancer cells, significantly enhancing the proportion of cell death. In conclusion, this study proposes that the genetic or pharmacological inhibition of IRP2 in BC cells may serve as a novel therapeutic strategy for increasing radiosensitivity and overcoming resistance by inducing mitochondrial dysfunction.