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.
肿瘤细胞治疗研究
英文原题:The effects of Stem Cell-Conditioned Media on Malignancy Behavior of Breast Cancer Cells in Vitro.
The effects of Stem Cell-Conditioned Media on Malignancy Behavior of Breast Cancer Cells in Vitro.
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乳腺癌是全球女性中最常被诊断出的癌症类型。近年来,研究人员对探索替代治疗方法(包括干细胞疗法)的兴趣显著增加。本研究旨在体外探讨脂肪来源间充质干细胞条件培养基(AD-MSCs-CM)对乳腺癌细胞(MDA-MB-231)凋亡诱导和迁移抑制的影响。
在本研究中,恶性乳腺癌细胞(MDA-MB-231)和脂肪来源间充质干细胞(AD-MSCs)分别在DMEM/F12/FBS(15%)培养基中于标准条件下单独培养。随后,将来源于AD-MSCs的条件培养基加入MDA-MB-231细胞中。在暴露24小时和48小时后,使用定量逆转录聚合酶链反应(qRT-PCR)检测CASP3、KRAS和MMP9的表达水平。
此外,分别使用MTT和伤口愈合实验评估癌细胞的增殖和迁移能力。此外,使用western blot检测Caspase-3、K-RAS和MMP-9的蛋白表达。
值得注意的是,在MDA-MB-231细胞中,AD-MSCs-CM处理后MMP9和KRAS基因的表达水平显著降低。此外,发现治疗组中CASP3基因表达水平显著升高。
另外,通过MTT和伤口愈合实验,经AD-MSCs-CM处理的MDA-MB-231细胞的增殖明显减弱。此外,观察到AD-MSCs-CM可诱导caspase-3活化并降低K-RAS和MMP-9的蛋白表达。
本研究结果表明,AD-MSCs-CM可能对乳腺癌细胞的凋亡、增殖和迁移产生影响。因此,它可被提出作为一种有前景的抑制乳腺癌的治疗策略。
然而,仍需进一步的测试和研究来验证这些发现,并确定该方法的全部潜力。
Breast cancer represents the most frequently diagnosed form of cancer among women on a global scale. In recent years, there has been a notable increase in interest among researchers in exploring alternative therapeutic methods, including stem cell therapy. The objective of this study was to examine the impact of adipose-derived mesenchymal stem cell-conditioned media (AD-MSCs-CM) on apoptosis induction and migration inhibition of breast cancer cells (MDA-MB-231) in vitro .
In this study, malignant breast cancer cells (MDA-MB-231) and adipose-derived mesenchymal stem cells (AD-MSCs) were cultured separately in DMEM/F12/FBS (15%) culture media under standard conditions. Subsequently, the conditioned media derived from AD-MSCs was introduced to the MDA-MB-231 cells. Following a 24- and 48-hour exposure period, the expression levels of CASP3, KRAS, and MMP9 were evaluated using a quantitative reverse transcription polymerase chain reaction (qRT-PCR) assay.
Furthermore, the proliferation and migration abilities of the cancer cells were evaluated using MTT and wound healing assays, respectively.
Furthermore, the protein expression of Caspase-3, K-RAS, and MMP-9 was examined using a western blot assay. It is noteworthy that the expression levels of the MMP9 and KRAS genes were significantly reduced following treatment with AD-MSCs-CM in MDA-MB-231 cells.
Furthermore, the CASP3 gene expression level was found to have increased significantly in the treated groups.
Additionally, the proliferation of MDA-MB-231 cells treated with AD-MSCs-CM was markedly diminished by MTT and wound healing assays.
Moreover, the AD-MSCs-CM was observed to induce caspase-3 activation and reduce the protein expression of K-RAS and MMP-9. The results of this study indicate that AD-MSCs-CM may exert an influence on the apoptosis, proliferation, and migration of breast cancer cells. Consequently, it could be proposed as a promising therapeutic strategy for the suppression of breast cancer.
However, further testing and research are required to validate these findings and to ascertain the full potential of this approach.
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