Osteosarcoma (OS) is the most common primary malignant bone tumour in children and adolescents. The long‐term survival rate of OS patients is stubbornly low mainly due to the chemotherapy resistance. We therefore aimed to investigate the antitumoral effects and underlying mechanisms of proanthocyanidin B2 (PB2) on OS cells in the current study. The effect of PB2 on the proliferation and apoptosis of OS cell lines was assessed by CCK‐8, colony formation, and flow cytometry assays. The target gene and protein expression levels were measured by qRT‐PCR and Western blotting. A xenograft mouse model was established to assess the effects of PB2 on OS proliferation and apoptosis in vivo. Results from in vitro experiments showed that PB2 inhibited the proliferation and induced apoptosis of OS cells, and also increased the expression levels of apoptosis‐related proteins. Moreover, PB2 induced OS cell apoptosis through suppressing the PI3K/AKT signalling pathway. The in vivo experiments further confirmed that PB2 could inhibit OS tumour growth and induce its apoptosis. Taken together, these results suggested that PB2 inhibited the proliferation and induced apoptosis of OS cells through the suppression of the PI3K/AKT signalling pathway.

中文翻译：

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原花青素B2通过抑制PI3K / AKT途径抑制增殖并诱导骨肉瘤细胞凋亡。

骨肉瘤（OS）是儿童和青少年中最常见的原发性恶性骨肿瘤。OS患者的长期生存率顽固地较低，这主要归因于化疗耐药性。因此，我们旨在研究当前研究中原花青素B2（PB2）对OS细胞的抗肿瘤作用及其潜在机制。通过CCK-8，集落形成和流式细胞术分析评估了PB2对OS细胞系增殖和凋亡的影响。通过qRT-PCR和Western blotting测定靶基因和蛋白质表达水平。建立异种移植小鼠模型以评估PB2对体内OS增殖和凋亡的影响。体外实验结果表明PB2抑制OS细胞的增殖并诱导其凋亡，并且还增加了凋亡相关蛋白的表达水平。此外，PB2通过抑制PI3K / AKT信号传导途径诱导OS细胞凋亡。体内实验进一步证实PB2可以抑制OS肿瘤的生长并诱导其凋亡。综上所述，这些结果表明PB2通过抑制PI3K / AKT信号传导途径抑制OS细胞的增殖并诱导其凋亡。