克洛西汀通过多途径抑制增强替莫唑胺对胶质母细胞瘤的疗效

Wei-En Tsai, Yen-Tsen Liu, Fu-Hsuan Kuo, Wen-Yu Cheng, Chiung-Chyi Shen, Ming-Tsang Chiao, Yu-Fen Huang, Yea-Jiuen Liang, Yi-Chin Yang, Wan-Yu Hsieh, Jun-Peng Chen, Szu-Yuan Liu, Cheng-Di Chiu
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引用次数: 0

摘要

背景:多形性胶质母细胞瘤(GBM多形性胶质母细胞瘤(GBM)是一种侵袭性脑肿瘤,很难通过手术切除。研究表明,藏红花中的物质,即藏红花素和藏红花苷,可以成为有效的天然疗法,显示出杀死癌细胞的能力:我们的研究重点是利用 U87 细胞系评估藏红花素对神经胶质瘤的影响。我们特别研究了藏红花素如何影响胶质瘤细胞的存活、生长和扩散,探讨了其在 75-150 μM 浓度范围内的影响。研究还包括藏红花素与化疗药物替莫唑胺(TMZ)的联合实验,以评估潜在的协同效应:结果:西红花素能明显降低胶质瘤细胞的活力、增殖和迁移。它通过降低基质金属肽酶9(MMP-9)和Ras同源家族成员A(RhoA)的水平来达到上述效果。此外,藏红花酸还能抑制肿瘤生长所需的细胞结构的形成。它阻断了对癌细胞存活至关重要的 Ak Strain Transforming(AKT)信号通路的多个点。这种治疗方法增加了胶质瘤细胞的死亡并破坏了细胞周期。在与 TMZ 联合使用时,西西替酯不仅能增强减少癌细胞生长的作用,还能促进细胞死亡和减少细胞复制。这种联合疗法进一步降低了高迁移率基团框 1(HMGB1)和高级糖化终产物受体(RAGE)的水平,这些蛋白与炎症和肿瘤进展有关。它选择性地抑制了参与细胞应激反应的某些途径,而不影响其他途径:我们的研究结果凸显了西番莲素治疗胶质瘤的潜力。它针对肿瘤生长和扩散的各种机制,提供了多种治疗途径。进一步的研究对于充分了解和利用藏红花素治疗胶质瘤的益处至关重要。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Crocetin Enhances Temozolomide Efficacy in Glioblastoma Therapy Through Multiple Pathway Suppression.

Background: Glioblastoma multiforme (GBM) is an aggressive type of brain tumor that is difficult to remove surgically. Research suggests that substances from saffron, namely crocetin and crocin, could be effective natural treatments, showing abilities to kill cancer cells.

Methods: Our study focused on evaluating the effects of crocetin on glioma using the U87 cell line. We specifically investigated how crocetin affects the survival, growth, and spread of glioma cells, exploring its impact at concentrations ranging from 75-150 μM. The study also included experiments combining crocetin with the chemotherapy drug Temozolomide (TMZ) to assess potential synergistic effects.

Results: Crocetin significantly reduced the viability, proliferation, and migration of glioma cells. It achieved these effects by decreasing the levels of Matrix Metallopeptidase 9 (MMP-9) and Ras homolog family member A (RhoA), proteins that are critical for cancer progression. Additionally, crocetin inhibited the formation of cellular structures necessary for tumor growth. It blocked multiple points of the Ak Strain Transforming (AKT) signaling pathway, which is vital for cancer cell survival. This treatment led to increased cell death and disrupted the cell cycle in the glioma cells. When used in combination with TMZ, crocetin not only enhanced the reduction of cancer cell growth but also promoted cell death and reduced cell replication. This combination therapy further decreased levels of high mobility group box 1 (HMGB1) and Receptor for Advanced Glycation End-products (RAGE), proteins linked to inflammation and tumor progression. It selectively inhibited certain pathways involved in the cellular stress response without affecting others.

Conclusion: Our results underscore the potential of crocetin as a treatment for glioma. It targets various mechanisms involved in tumor growth and spread, offering multiple avenues for therapy. Further studies are essential to fully understand and utilize crocetin's benefits in treating glioma.

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