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雷公藤甲素通过上调SW1353人软骨肉瘤细胞中miR-125a-5p靶向PI3K/Akt信号通路,抑制细胞迁移和活力,并促进细胞凋亡。

Triptolide inhibits migration and viability, and promotes apoptosis by targeting the PI3K/Akt signaling pathway via upregulation of miR‑125a‑5p in SW1353 human chondrosarcoma cells.

作者信息

Liang Chaoyi, Zhuoer Zhang, Yuan Liu, Bing Zhang

机构信息

Department of Orthopedics, Affiliated Hospital of Jiangxi University of Chinese Medicine, Nanchang, Jiangxi 330006, P.R. China.

出版信息

Mol Med Rep. 2025 Jun;31(6). doi: 10.3892/mmr.2025.13514. Epub 2025 Apr 11.

Abstract

Malignant chondrosarcoma is a rare type of bone cancer, for which an effective comprehensive treatment strategy is lacking. Triptolide (TPL) is an active chemical component originating from the Chinese herb Hook F, which exerts inhibitory effects on various cancer cells. However, to the best of our knowledge, little is currently known about the effect of TPL on chondrosarcoma. In the present study, SW1353 human chondrosarcoma cells were used as cell model. Cell Counting Kit‑8, Annexin V/PI staining, wound healing assay, Transwell invasion assay and the detection of proinflammatory cytokines were performed to determine the effects of TPL on SW1353 chondrosarcoma cell viability, apoptosis, migration, invasion and inflammation. In addition, the protein expression levels of phosphorylated (p)‑PI3K, PI3K, p‑AKT and AKT were detected to determine whether TPL exerted its antitumor effects via the PI3K/Akt signaling pathway. Furthermore, the microRNA (miR)‑125a‑5p‑inhibitor was introduced into cells to determine whether TPL exerted its effect on SW1353 cells via miR‑125a‑5p. TPL inhibited SW1353 chondrosarcoma cell viability, migration, invasion and proinflammatory cytokine expression in a dose‑dependent manner. The most obvious effect observed in the current study was in the 50 nM TPL group. In addition, TPL inhibited PI3K/Akt signaling pathway activation and upregulated miR‑125a‑5p expression in a dose‑dependent manner. By contrast, miR‑125‑5p inhibition accelerated the viability, migration, invasion and proinflammatory cytokine expression of SW1353 cells compared with the control. Notably, miR‑125a‑5p inhibition reversed the effects of TPL on SW1353 cells. In conclusion, TPL exerted an antitumor effect on SW1353 human chondrosarcoma cells and miR‑125a‑5p served an essential role in inhibiting the tumorigenic phenotype of chondrosarcoma cells. TPL exerted its inhibitory effects on chondrosarcoma cells via upregulating miR‑125a‑5p and inhibiting the PI3K/Akt signaling pathway.

摘要

恶性软骨肉瘤是一种罕见的骨癌,目前缺乏有效的综合治疗策略。雷公藤甲素(TPL)是一种源自中药雷公藤的活性化学成分,对多种癌细胞具有抑制作用。然而,据我们所知,目前关于TPL对软骨肉瘤的作用了解甚少。在本研究中,使用SW1353人软骨肉瘤细胞作为细胞模型。通过细胞计数试剂盒-8、膜联蛋白V/碘化丙啶染色、伤口愈合试验、Transwell侵袭试验以及促炎细胞因子检测,来确定TPL对SW1353软骨肉瘤细胞活力、凋亡、迁移、侵袭和炎症的影响。此外,检测磷酸化(p)-PI3K、PI3K、p-AKT和AKT的蛋白表达水平,以确定TPL是否通过PI3K/Akt信号通路发挥其抗肿瘤作用。此外,将微小RNA(miR)-125a-5p抑制剂导入细胞,以确定TPL是否通过miR-125a-5p对SW1353细胞发挥作用。TPL以剂量依赖性方式抑制SW1353软骨肉瘤细胞活力、迁移、侵袭和促炎细胞因子表达。在本研究中观察到的最明显效果出现在50 nM TPL组。此外,TPL以剂量依赖性方式抑制PI3K/Akt信号通路激活并上调miR-125a-5p表达。相比之下,与对照组相比,miR-125-5p抑制加速了SW1353细胞的活力、迁移、侵袭和促炎细胞因子表达。值得注意的是,miR-125a-5p抑制逆转了TPL对SW1353细胞的作用。总之,TPL对SW1353人软骨肉瘤细胞发挥抗肿瘤作用,miR-125a-5p在抑制软骨肉瘤细胞致瘤表型中起重要作用。TPL通过上调miR-125a-5p并抑制PI3K/Akt信号通路对软骨肉瘤细胞发挥抑制作用。

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