Mechanism of Baclofen Inhibiting the Proliferation and Metastasis of GBM by Regulating YAP | Zendy

Lin Zhu | Zendy; Juan Lu | Zendy; Zhijun Bao | Zendy; ShiWen Guo | Zendy

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Mechanism of Baclofen Inhibiting the Proliferation and Metastasis of GBM by Regulating YAP

Author(s) -

Lin Zhu,

Juan Lu,

Zhijun Bao,

ShiWen Guo

Publication year - 2021

Publication title -

journal of chemistry

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.436

H-Index - 50

eISSN - 2090-9063

pISSN - 2090-9071

DOI - 10.1155/2021/2753571

Subject(s) - baclofen , chemistry , phosphorylation , survivin , apoptosis , cancer research , cell growth , in vivo , pharmacology , receptor , biochemistry , medicine , biology , agonist , microbiology and biotechnology

This study explores the effect of baclofen on the malignant phenotype of glioblastoma (GBM) and the growth of xenograft tumors and investigates the related mechanisms, aiming to reveal the effect of baclofen on the occurrence and development of GBM. The development of new therapeutic drugs for GBM lays a theoretical and experimental foundation. Research results show that baclofen could inhibit GBM cell proliferation and migration and promote GBM cell apoptosis; baclofen dose- and time-dependently could induce GBM cell YAP phosphorylation. YAP participated in the effect of baclofen on GBM cell proliferation and migration inhibition. Baclofen induced YAP phosphorylation in GBM cells through the GABABR2-Gs-Lats1/2 signaling pathway. Baclofen could inhibit the expression of survivin and Bcl2. Baclofen inhibits subcutaneous tumors by inducing YAP phosphorylation in vivo.

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