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<p>This study aimed to evaluate the biological effects of sevoflurane and desflurane on breast cancer cell lines representing different molecular subtypes under in vitro conditions. Specifically, the effects of these inhalational anesthetic agents on parameters associated with cancer progression, including cell proliferation, colony formation, apoptosis, and migration, were comparatively investigated. Triple-negative breast cancer cells (MDA-MB-231), estrogen receptor-positive cells (MCF-7), and non-tumorigenic breast epithelial cells (MCF-10&#xa0;A) were used. Cells were exposed to clinically relevant concentrations of sevoflurane (3.6%) and desflurane (10.3%) for 3&#xa0;h, followed by 24&#xa0;h of incubation. Cell viability (MTS assay), colony formation, wound healing (migration), Annexin V apoptosis analysis, and Western blot analysis of apoptosis-related proteins were performed. Exposure to desflurane and sevoflurane significantly reduced the viability of MDA-MB-231 and MCF-7 cells (<i>p</i> &lt; 0.0001), whereas no significant change was observed in MCF-10&#xa0;A cells. Colony formation was significantly suppressed only in MDA-MB-231 cells, with a more pronounced effect observed following desflurane exposure. Neither agent significantly affected cell migration. Apoptosis rates significantly increased in MDA-MB-231 cells treated with desflurane (<i>p</i> &lt; 0.0001). Western blot analysis demonstrated that desflurane increased p53 expression in MDA-MB-231 cells, whereas sevoflurane reduced its expression; no significant alterations were observed in PARP-1 and AIF levels. These findings suggest that desflurane exerts proliferation-inhibitory and apoptosis-inducing effects, particularly in triple-negative breast cancer cells. Sevoflurane demonstrated comparatively weaker effects. Overall, our results indicate that volatile anesthetics may directly influence cancer cell biology; however, their clinical implications require further validation in in vivo and clinical studies.</p>

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Research on the effects of desflurane and sevoflurane on proliferation and migration of breast cancer cells

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月9日

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  • Oğuz Kaan Şimşek,
  • Aliye Çoruh,
  • Ahsen Güler,
  • Ayşe Doğa Karipçin,
  • Zühal Hamurcu

摘要

This study aimed to evaluate the biological effects of sevoflurane and desflurane on breast cancer cell lines representing different molecular subtypes under in vitro conditions. Specifically, the effects of these inhalational anesthetic agents on parameters associated with cancer progression, including cell proliferation, colony formation, apoptosis, and migration, were comparatively investigated. Triple-negative breast cancer cells (MDA-MB-231), estrogen receptor-positive cells (MCF-7), and non-tumorigenic breast epithelial cells (MCF-10 A) were used. Cells were exposed to clinically relevant concentrations of sevoflurane (3.6%) and desflurane (10.3%) for 3 h, followed by 24 h of incubation. Cell viability (MTS assay), colony formation, wound healing (migration), Annexin V apoptosis analysis, and Western blot analysis of apoptosis-related proteins were performed. Exposure to desflurane and sevoflurane significantly reduced the viability of MDA-MB-231 and MCF-7 cells (p < 0.0001), whereas no significant change was observed in MCF-10 A cells. Colony formation was significantly suppressed only in MDA-MB-231 cells, with a more pronounced effect observed following desflurane exposure. Neither agent significantly affected cell migration. Apoptosis rates significantly increased in MDA-MB-231 cells treated with desflurane (p < 0.0001). Western blot analysis demonstrated that desflurane increased p53 expression in MDA-MB-231 cells, whereas sevoflurane reduced its expression; no significant alterations were observed in PARP-1 and AIF levels. These findings suggest that desflurane exerts proliferation-inhibitory and apoptosis-inducing effects, particularly in triple-negative breast cancer cells. Sevoflurane demonstrated comparatively weaker effects. Overall, our results indicate that volatile anesthetics may directly influence cancer cell biology; however, their clinical implications require further validation in in vivo and clinical studies.