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<p>Hypoxia is associated with radiation resistance in diverse tumors. Aloe-emodin (AE) has a wide range of pharmacological effects, including anti-tumor activity. The present study aims to determine whether AE can mediate cell radioresistance by regulating hypoxia-inducible factor-1 α (HIF-1α) levels in SU-DHL-4 cells. Analysis of the effect of AE on radiation resistance and hypoxia-induced radiation resistance in SU-DHL-4 cells by cell counting kit-8, clonogenic, and transwell migration assays. Loss-of-function experiments were performed to analyze the effect of HIF-1α knockdown on AE-mediated radiation sensitivity in hypoxia-stimulated SU-DHL-4 cells under radiation. AE significantly decreased the activity of SU-DHL-4 cells in a concentration- dependent manner, and the combination of AE with radiation markedly repressed the proliferation and migrating capacities of SU-DHL-4 cells. AE lessened hypoxia-trigged radiation resistance in SU-DHL-4. Whether under normal or hypoxic conditions, HIF-1α protein levels in SU-DHL-4 cells were progressively up-regulated with the elevation of radiation doses; however, up-regulated HIF-1α protein levels were weakened after AE treatment. Importantly, AE significantly decreased cell proliferation and migration in SU-DHL-4 cells under the simultaneous existence of hypoxia and radiation. However, AE lightly decreased cell proliferation in HIF-1α-silenced SU-DHL-4 cells under the same conditions but did not significantly affect cell migration, implying that AE improved hypoxia-induced radiation resistance by interacting with HIF-1α in SU-DHL-4 cells. AE improved hypoxia-induced radioresistance by interacting with HIF-1α in SU-DHL-4 cells, providing a theoretical basis for AE as a drug for treating diffuse large B-cell lymphoma.</p>

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Aloe-Emodin Decreases the Hypoxia-Induced Radioresistance by Interacting with Hypoxiainducible Factor-1 α in SU-DHL-4 Cells

  • 期刊论文

  • 发表日期：

    2025年1月1日

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  • Lili Zhang,
  • Xiaojie Wang,
  • Yue Zhang,
  • Hui Gao,
  • Yanxia He,
  • Mengmeng Liu

摘要

Hypoxia is associated with radiation resistance in diverse tumors. Aloe-emodin (AE) has a wide range of pharmacological effects, including anti-tumor activity. The present study aims to determine whether AE can mediate cell radioresistance by regulating hypoxia-inducible factor-1 α (HIF-1α) levels in SU-DHL-4 cells. Analysis of the effect of AE on radiation resistance and hypoxia-induced radiation resistance in SU-DHL-4 cells by cell counting kit-8, clonogenic, and transwell migration assays. Loss-of-function experiments were performed to analyze the effect of HIF-1α knockdown on AE-mediated radiation sensitivity in hypoxia-stimulated SU-DHL-4 cells under radiation. AE significantly decreased the activity of SU-DHL-4 cells in a concentration- dependent manner, and the combination of AE with radiation markedly repressed the proliferation and migrating capacities of SU-DHL-4 cells. AE lessened hypoxia-trigged radiation resistance in SU-DHL-4. Whether under normal or hypoxic conditions, HIF-1α protein levels in SU-DHL-4 cells were progressively up-regulated with the elevation of radiation doses; however, up-regulated HIF-1α protein levels were weakened after AE treatment. Importantly, AE significantly decreased cell proliferation and migration in SU-DHL-4 cells under the simultaneous existence of hypoxia and radiation. However, AE lightly decreased cell proliferation in HIF-1α-silenced SU-DHL-4 cells under the same conditions but did not significantly affect cell migration, implying that AE improved hypoxia-induced radiation resistance by interacting with HIF-1α in SU-DHL-4 cells. AE improved hypoxia-induced radioresistance by interacting with HIF-1α in SU-DHL-4 cells, providing a theoretical basis for AE as a drug for treating diffuse large B-cell lymphoma.