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首页> 外文期刊>Journal of International Medical Research >Tizanidine hydrochloride exhibits a cytotoxic effect on osteosarcoma cells through the PI3K/AKT signaling pathway
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Tizanidine hydrochloride exhibits a cytotoxic effect on osteosarcoma cells through the PI3K/AKT signaling pathway

机译：盐酸替扎尼定通过PI3K / AKT信号通路对骨肉瘤细胞具有细胞毒性作用

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Objectives α2-adrenergic receptors are reportedly involved in cancer cell proliferation, invasion, and apoptosis through regulation of diverse molecules, which implies that it contributes to tumor progression. However, the functional significance of α2-adrenergic receptors in osteosarcoma (OS) is unclear. Tizanidine hydrochloride (THC), an α2-adrenergic receptor agonist, is often used to alleviate symptoms of spasticity. This study investigated the functional implications of THC treatment on human OS cells and the underlying mechanisms of resulting changes. Methods The proliferation of U2 OS cells was assessed by Cell Counting Kit-8; the migration and invasion capacities of U2 OS cells were then analyzed by transwell assay. Moreover, apoptosis in U2 OS cells was evaluated by flow cytometry and western blot analyses. Additionally, expression levels of key proteins in the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT) signaling pathway were measured. Results THC inhibited the proliferation, migration, and invasion of U2 OS cells, but promoted apoptosis within these cells. Expression levels of p-AKT, p-mTOR, and p-P70S6K were reduced by exposure to THC, suggesting involvement of PI3K/AKT signaling in THC-induced cytotoxicity within OS cells. Conclusions THC may play a novel role in OS cell cytotoxicity, and these findings suggest a potent therapeutic strategy for OS treatment.
机译：目的据报道，α2-肾上腺素能受体通过调节多种分子而参与癌细胞的增殖，侵袭和凋亡，这暗示它促进了肿瘤的发展。然而，尚不清楚α2-肾上腺素能受体在骨肉瘤（OS）中的功能意义。盐酸替扎尼定（THC）是一种α2-肾上腺素能受体激动剂，通常用于缓解痉挛症状。这项研究调查了THC治疗对人类OS细胞的功能含义以及导致变化的潜在机制。方法用细胞计数试剂盒8（Cell Counting Kit-8）评估U2 OS细胞的增殖。然后通过transwell分析法分析U2 OS细胞的迁移和侵袭能力。此外，通过流式细胞术和蛋白质印迹分析评估了U2 OS细胞的凋亡。此外，还测量了磷脂酰肌醇3-激酶（PI3K）/蛋白激酶B（AKT）信号通路中关键蛋白的表达水平。结果THC抑制U2 OS细胞的增殖，迁移和侵袭，但促进U2 OS细胞凋亡。暴露于THC会降低p-AKT，p-mTOR和p-P70S6K的表达水平，表明PI3K / AKT信号传导参与THC诱导的OS细胞内细胞毒性。结论THC可能在OS细胞的细胞毒性中起着新的作用，这些发现提示了OS治疗的有效治疗策略。

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