间充质干细胞（MSC）和癌症干细胞（CSC）在癌症进展和治疗反应中发挥着关键作用。本研究旨在探讨紫杉醇诱导的 MSC 对表达 CD44 /CD24- 表型的 CSC 的影响，重点关注 Nrf2 调节和凋亡诱导。分别进行流式细胞术。使用 MACS 从 MDA-MB-231 中分离 CSC，并根据形态和 CD44 /CD24- 表达进行表征。共培养实验使用 MTT 测定评估了紫杉醇诱导的 MSC 对 CSC 活力的细胞毒性作用。流式细胞术分析通过膜联蛋白V-PI染色评估细胞凋亡诱导，并通过qRT-PCR分析测量Nrf2和Caspase-3基因表达。MSC表现出典型的粘附和分化能力，证实了其间充质谱系。 CSCs 表现出细长的形态并表达 CD44 /CD24-，这是茎样行为的特征。紫杉醇诱导 MSC 中剂量依赖性 Nrf2 基因表达。与紫杉醇诱导的 MSC 共培养以剂量依赖性方式降低 CSC 活力，在 MSCs:CSC 比例为 5:1 时观察到显着降低。与单独紫杉醇治疗相比，共培养降低了 CSC 中的 Nrf2 基因表达并增加了细胞凋亡，其中 caspase-3 基因表达更高。紫杉醇诱导的 MSC 降低了 Nrf2 表达并显着降低了 CSC 活力，同时增强了细胞凋亡。这表明了减轻 CD44 /CD24- CSC 中紫杉醇耐药性的潜在策略。利用紫杉醇诱导的 MSC 为靶向 Nrf2 和促进 CSC 细胞凋亡提供了一条有前途的途径，有可能提高化疗的疗效并解决癌症治疗中的耐药机制。© 2024 Hermansyah 等人。

Mesenchymal Stem Cells (MSCs) and Cancer Stem Cells (CSC) play pivotal roles in cancer progression and therapeutic responses. This study aimed to explored the effect of MSCs induced by paclitaxel on CSC expressing the CD44+/CD24- phenotype, focusing on Nrf2 modulation and apoptosis induction.MSCs were characterized for adherence, differentiation potential, and surface markers via standard culture, staining assays, and flow cytometry, respectively. CSCs isolated from MDA-MB-231 using MACS and were characterized based on morphology and CD44+/CD24- expression. Co-culture experiments evaluated the cytotoxic effect of Paclitaxel-induced MSCs on CSC viability using MTT assays. Flow cytometry analysis assessed apoptosis induction via annexin V-PI staining and Nrf2 and Caspase-3 gene expression were measure by qRT-PCR analysis.MSCs exhibited typical adherence and differentiation capabilities, confirming their mesenchymal lineage. CSCs displayed an elongated morphology and expressed CD44+/CD24-, characteristic of stem-like behavior. Paclitaxel induced dose-dependent Nrf2 gene expression in MSCs. Co-culture with Paclitaxel-induced MSCs reduced CSC viability in a dose-dependent manner, with a significant decrease observed at a 5:1 MSCs:CSC ratio. Co-culture decreased the Nrf2 gene expression and increased apoptosis in CSCs, with higher caspase-3 gene expression compared to solitary paclitaxel treatment.Paclitaxel-induced MSCs decreased Nrf2 expression and significantly decreased CSC viability while enhancing apoptosis. This suggests a potential strategy to mitigate paclitaxel resistance in CD44+/CD24- CSCs. Leveraging Paclitaxel-induced MSCs presents a promising avenue for targeting Nrf2 and promoting apoptosis in CSCs, potentially improving the efficacy of chemotherapy and addressing resistance mechanisms in cancer treatment.© 2024 Hermansyah et al.