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SAS口腔鳞状细胞癌与MCF-7乳腺癌细胞对BNCT的差异性放射生物学反应

Distinct Radiobiological Responses to BNCT in SAS Oral Squamous Cell Carcinoma and MCF-7 Breast Cancer Cells

Yuxiang Zhao, Zhao Sun, Changming Wang, Jianghao Lai, Jie Zhou, Zhencen He, Zhimin Hu

arXiv 2609.05931首次发表:更新:

AI 中文总结

本研究比较SAS口腔鳞癌和MCF-7乳腺癌细胞对BNCT的放射生物学反应,发现两者在克隆形成抑制、细胞周期阻滞和凋亡上存在差异,表明BNCT敏感性受硼积累和细胞特异性特征共同影响。

AI 中文摘要

本研究比较了SAS口腔鳞状细胞癌细胞和MCF-7乳腺癌细胞在接受基于加速器的硼中子俘获治疗(BNCT)后的放射生物学反应。通过质子束轰击锂靶产生中子,随后经过慢化获得足够的热中子用于BNCT照射。采用硼苯丙氨酸(BPA)作为硼递送剂。通过γ-H2AX免疫荧光染色、细胞周期分析、凋亡分析和克隆形成存活实验评估BNCT诱导的生物学反应。BNCT在两种细胞系中均诱导了显著的γ-H2AX焦点形成,表明照射后产生了与DNA损伤相关的反应。两种细胞系在照射后的结局上表现出明显差异。SAS细胞表现出更强的克隆形成抑制和显著的G2/M期积累,而MCF-7细胞则表现出持续的G0/G1期积累和延迟的凋亡。这些结果表明,BNCT敏感性由硼积累和细胞系特异性生物学特征共同决定。本研究提供了实验证据,强调了肿瘤依赖性细胞反应在理解和优化BNCT疗效中的重要性。

英文摘要

This work compared the radiobiological responses of SAS oral squamous cell carcinoma cells and MCF-7 breast cancer cells following accelerator-based boron neutron capture therapy (BNCT). Neutrons were generated by bombarding a lithium target with proton beams, followed by moderation to obtain sufficient thermal neutrons for BNCT irradiation. Boronophenylalanine (BPA) was used as the boron delivery agent. BNCT-induced biological responses were evaluated by gamma-H2AX immunofluorescence staining, cell-cycle analysis, apoptosis analysis, and clonogenic survival assays. BNCT induced marked gamma-H2AX foci formation in both cell lines, indicating DNA damage-associated responses after irradiation. The two cell lines further showed distinct post-irradiation outcomes. SAS cells exhibited stronger clonogenic suppression and prominent G2/M accumulation, whereas MCF-7 cells showed sustained G0/G1 accumulation and delayed apoptosis. These results suggest that BNCT sensitivity is determined by both boron accumulation and cell-line-specific biological characteristics. This work provides experimental evidence highlighting the importance of tumor-dependent cellular responses in understanding and optimizing BNCT efficacy.

Comments10 pages, 6 figures, 1 table; supplementary information included

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