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J Cancer. 2019 Jul 25;10(19):4499-4508. doi: 10.7150/jca.31487. eCollection 2019.

Galangin inhibits epithelial-mesenchymal transition and angiogenesis by downregulating CD44 in glioma.

Author information

1
Department of Neurosurgery, Shunde Hospital, Southern Medical University (The First People,s Hospital of Shunde Foshan), Foshan, China.
2
Department of Neurosurgery, Shanwei People's Hospital, Shanwei, Guangdong, China.

Abstract

Galangin (3,5,7‑trihydroxyflavone), a natural flavonoid present in plants, has been reported to possess anticancer properties in various types of cancers comprising glioma. The underlying mechanism, however, has not been fully elucidated. CD44, a hall marker in glioma, has been reported to be associated with epithelial-mesenchymal transition (EMT) and angiogenesis, which play important roles in glioma progression. In this study, we aimed to investigate whether galangin can inhibit EMT, angiogenesis and CD44 expression in glioma. We observed that galangin inhibited the proliferation, migration, invasion and angiogenesis of glioma cells in a dose-dependent manner, suppressed the expression of CD44 and inhibited angiogenesis of glioma cells through downregulating vascular endothelial growth factor (VEGF) in HUVECs. In addition, the overexpression of CD44 in U87 and U251 cells partly abolished the effects of galangin on glioma cells. Moreover, galangin suppressed tumor growth in an intracranial glioma mouse model. These results indicate that galangin is a potential novel drug for glioblastoma treatment due to its ability to suppress of CD44, EMT and angiogenesis.

KEYWORDS:

CD44; EMT; galangin; glioblastoma; suppression

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