Department of Traditional Chinese Medicine, The First Affiliated Hospital of Xinjiang Medical University, No. 137 Liyushan South Road, Ürümqi, 830011, Xinjiang, China.
Biotechnol Lett. 2021 Jun;43(6):1229-1240. doi: 10.1007/s10529-021-03081-6. Epub 2021 Feb 3.
Bufalin is an active component of the traditional Chinese medicine "Chan Su" and is reported to play anti-tumor roles in cancer development, but its functional mechanism is largely unclear. This study intends to explore a potential action mode of bufalin in NSCLC.
The malignant properties of NSCLC, including cell viability, proliferation, adhesion capacity, migration and invasion, were monitored by cell counting kit-8 (CCK-8), adhesion assay and transwell assay, respectively. The expression of circ_0046264 and miR-522-3p was detected by quantitative real-time polymerase chain reaction (qRT-PCR). The expression of proliferation- and migration-related markers was examined by western blot. The putative relationship between circ_0046264 and miR-522-3p was verified by dual-luciferase reporter assay, RIP assay and RNA pull-down assay. Animal experiments in nude mice were performed to investigate the role of bufalin in vivo.
Bufalin treatment inhibited cell viability, colony formation, cell adhesion capacity, migration and invasion in NSCLC cells. Bufalin facilitated the expression of circ_0046264, and circ_0046264 overexpression also inhibited NSCLC cell viability, colony formation, cell adhesion capacity, migration and invasion. Besides, circ_0046264 knockdown partially counteracted the effects of bufalin. Further, miR-522-3p was identified as a target of circ_0046264, and its deficiency reversed the effects of circ_0046264 knockdown to suppress malignant activities of NSCLC cells. In addition, bufalin restrained the tumor growth and development in vivo via enhancing the expression of circ_0046264.
Bufalin played an anti-tumor role in NSCLC by modulating the circ_0046264/miR-522-3p pathway, which might be a potential functional mechanism of bufalin in NSCLC.
蟾毒灵是中药“蟾酥”的一种活性成分，据报道在癌症发展中具有抗肿瘤作用，但它的功能机制在很大程度上尚不清楚。本研究旨在探讨蟾毒灵在非小细胞肺癌（NSCLC）中的潜在作用模式。
通过细胞计数试剂盒-8（CCK-8）、黏附实验和 Transwell 实验分别监测 NSCLC 的恶性特性，包括细胞活力、增殖、黏附能力、迁移和侵袭。通过定量实时聚合酶链反应（qRT-PCR）检测 circ_0046264 和 miR-522-3p 的表达。通过 Western blot 检测增殖和迁移相关标志物的表达。通过双荧光素酶报告基因实验、RIP 实验和 RNA 下拉实验验证 circ_0046264 和 miR-522-3p 之间的假定关系。在裸鼠体内进行动物实验，以研究蟾毒灵在体内的作用。
蟾毒灵处理抑制了 NSCLC 细胞的活力、集落形成、细胞黏附能力、迁移和侵袭。蟾毒灵促进了 circ_0046264 的表达，circ_0046264 的过表达也抑制了 NSCLC 细胞的活力、集落形成、细胞黏附能力、迁移和侵袭。此外，circ_0046264 的敲低部分抵消了蟾毒灵的作用。此外，miR-522-3p 被鉴定为 circ_0046264 的靶标，其缺乏逆转了 circ_0046264 敲低抑制 NSCLC 细胞恶性活动的作用。此外，蟾毒灵通过增强 circ_0046264 的表达来抑制体内肿瘤的生长和发展。
蟾毒灵通过调节 circ_0046264/miR-522-3p 通路在 NSCLC 中发挥抗肿瘤作用，这可能是蟾毒灵在 NSCLC 中的潜在功能机制。
