基于 DNA 超分子水凝胶的保护性 NK 细胞储库用于增强三阴性乳腺癌治疗
Protective NK Cell Reservoir Based on DNA Supramolecular Hydrogel for Enhanced Triple-Negative Breast Cancer Therapy.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
英文原题:Apoptotic effects of human amniotic fluid mesenchymal stem cells conditioned medium on human MCF-7 breast cancer cell line.
Apoptotic effects of human amniotic fluid mesenchymal stem cells conditioned medium on human MCF-7 breast cancer cell line.
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我们的研究结果表明,hAFMSCs-CM 对 MCF-7 细胞具有凋亡效应;因此,应用 hAFMSCs-CM 作为治疗试剂,能够抑制乳腺癌细胞的活力并诱导凋亡。
乳腺癌作为女性最常见的恶性肿瘤,表现出高死亡率和化疗耐药性。研究表明,间充质干细胞在治疗癌症中可能具有抑制作用。因此,本研究使用人羊水间充质干细胞条件培养基(hAFMSCs-CM)作为凋亡试剂,作用于人MCF-7乳腺癌细胞系。
条件培养基(CM)由hAFMSCs制备。用CM处理MCF-7细胞后,采用多种分析方法(MTT、real-time PCR、western blot和流式细胞术)分别评估细胞活力、Bax和Bcl-2基因表达、P53蛋白表达以及细胞凋亡。人成纤维细胞(Hu02)用作阴性对照。此外,还进行了整合的meta分析方法。
MCF-7细胞在处理24小时(P < 0.0001)和72小时(P < 0.05)后活力显著降低。与对照细胞相比,用80% hAFMSCs-CM处理24小时后,Bax基因mRNA表达增加,Bcl-2 mRNA表达显著降低(分别为P = 0.0012,P < 0.0001);同时可观察到P53蛋白表达呈上升趋势。流式细胞术分析表明细胞发生凋亡。文献挖掘和整合meta分析结果显示,hAFMSCs-CM能够激活一个分子网络,其中Bcl2下调和P53、EIF5A、DDB2及Bax上调相协调,从而导致凋亡的激活。
Conditioned medium (CM) was prepared from hAFMSCs. After treating MCF-7 cells with CM, a number of analytical procedures (MTT, real-time PCR, western blot, and flow cytometry) were recruited to evaluate the cell viability, Bax and Bcl-2 gene expression, P53 protein expression, and apoptosis, respectively. Human fibroblast cells (Hu02) were used as the negative control. In addition, an integrated approach to meta-analysis was performed.
The MCF-7 cells' viability was decreased significantly after 24 hours ( P < 0.0001) and 72 hours ( P < 0.05) of treatment. Compared with the control cells, Bax gene's mRNA expression increased and Bcl-2's mRNA expression decreased considerably after treating for 24 hours with 80% hAFMSCs-CM ( P = 0.0012, P < 0.0001, respectively); an increasing pattern in P53 protein expression could also be observed. The flow cytometry analysis indicated apoptosis. Results from literature mining and the integrated meta-analysis showed that hAFMSCs-CM is able to activate a molecular network where Bcl2 downregulation stands in harmony with the upregulation of P53, EIF5A, DDB2, and Bax, leading to the activation of apoptosis.
Our finding demonstrated that hAFMSCs-CM presents apoptotic effect on MCF-7 cells; therefore, the application of hAFMSCs-CM, as a therapeutic reagent, can suppress breast cancer cells' viabilities and induce apoptosis.
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