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Proanthocyanidin B2 inhibits proliferation and induces apoptosis of osteosarcoma cells by suppressing the PI3K/AKT pathway

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 proanthocyani...

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Detalles Bibliográficos
Autores principales: Wu, Xinbo, Yu, Haiyang, Zhou, Haichao, Li, Zihua, Huang, Hui, Xiao, Fajiao, Xu, Shaochen, Yang, Yunfeng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7579710/
https://www.ncbi.nlm.nih.gov/pubmed/32914567
http://dx.doi.org/10.1111/jcmm.15818
Descripción
Sumario: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.