Cancer Biology Division, School of Biotechnology, Kalinga Institute of Industrial Technology (KIIT), Deemed to be University, Bhubaneswar, Odisha, 751024, India.
Nanomedicine (Lond). 2023 Jan;18(1):19-33. doi: 10.2217/nnm-2022-0243. Epub 2023 Mar 14.
This study aimed to explore the antiangiogenic mechanism of quinacrine-gold hybrid nanoparticle (QAuNP) and near-infrared (NIR) radiation in patient-derived primary breast cancer stem cells. Various cell-based angiogenesis and patient-derived xenograft mouse systems were used as models for the study. The experimental results showed that QAuNP + NIR treatment deregulated the HSP-70/TGF-β physical interaction in primary breast cancer stem cells. Reduced TGF-β secretion in the tumor microenvironment inhibited angiogenesis activation in endothelial cells by deregulating the TGF-β-mediated PI3K/AKT/mTOR cascade. This study revealed that QAuNP + NIR irradiation downregulated HSP-70 expression, inhibited the HSP-70/TGF-β interaction, reduced the secretion of TGF-β in the tumor microenvironment and ultimately inhibited TGF-β-mediated angiogenesis.
本研究旨在探索金吖啶酮-金混合纳米颗粒（QAuNP）与近红外（NIR）辐射在患者来源的原发性乳腺癌干细胞中的抗血管生成机制。 各种基于细胞的血管生成和患者来源的异种移植小鼠系统被用作该研究的模型。 实验结果表明，QAuNP+NIR 处理使 HSP-70/TGF-β 物理相互作用在原发性乳腺癌干细胞中失调。 肿瘤微环境中 TGF-β 分泌减少通过调节 TGF-β 介导的 PI3K/AKT/mTOR 级联来抑制内皮细胞中血管生成的激活。 本研究表明，QAuNP+NIR 照射下调 HSP-70 表达，抑制 HSP-70/TGF-β 相互作用，减少肿瘤微环境中 TGF-β 的分泌，最终抑制 TGF-β 介导的血管生成。
