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DOI 10.2174/0115665240284638240408081133

Медицинская библиотека · Current molecular medicine · 2025

Anlotinib Inhibiting Mantle Cell Lymphoma Proliferation and Inducing Apoptosis through PI3K/AKT/mTOR Pathway.

Wang Jiaping, Xu Zhijuan, Lai Yanli, Zhang Yanli, Zhang Ping, Mu Qitian, Yang Shujun, Sheng Lixia, Ouyang Guifang

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Аннотация

BACKGROUND

This study investigates the inhibitory mechanism of anlotinib on human Mantle Cell Lymphoma (MCL) cells through in vitro and in vivo experiments.

METHODS

In vitro cellular experiments validate the effects of anlotinib on MCL cell proliferation and apoptosis. Moreover, a subcutaneous xenograft nude mice model of Mino MCL cells was established to assess the anti-tumour effect and tumour microenvironment regulation of anlotinib in vivo.

RESULTS

The results indicate that MCL cell proliferation was significantly inhibited upon anlotinib exposure. The alterations in the expression of apoptosis-related proteins further confirm that anlotinib can induce apoptosis in MCL cells. Additionally, anlotinib significantly reduced the PI3K/Akt/mTOR phosphorylation level in MCL cells. The administration of a PI3K phosphorylation agonist, 740YP, could reverse the inhibitory effect of anlotinib on MCL. In the xenograft mouse model using Mino MCL cells, anlotinib treatment led to a gradual reduction in body weight and a significant increase in survival time compared to the control group. Additionally, anlotinib attenuated PD-1 expression and elevated inflammatory factors, CD4, and CD8 levels in tumour tissues.

CONCLUSION

Anlotinib effectively inhibits proliferation and induces apoptosis in MCL both in vitro and in vivo. This inhibition is likely linked to suppressing phosphorylation in the PI3K/Akt/mTOR pathway.

Для цитирования: Wang Jiaping, Xu Zhijuan, Lai Yanli, Zhang Yanli, Zhang Ping, Mu Qitian, Yang Shujun, Sheng Lixia, Ouyang Guifang. Anlotinib Inhibiting Mantle Cell Lymphoma Proliferation and Inducing Apoptosis through PI3K/AKT/mTOR Pathway.. Current molecular medicine. 2025. DOI: 10.2174/0115665240284638240408081133.

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