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Apigenin suppresses migration and invasion of transformed cells through down-regulation of C-X-C chemokine receptor 4 expression
Journal article   Open access   Peer reviewed

Apigenin suppresses migration and invasion of transformed cells through down-regulation of C-X-C chemokine receptor 4 expression

Lei Wang, Lisha Kuang, John Andrew Hitron, Young-Ok Son, Xin Wang, Amit Budhraja, Jeong-Chae Lee, Poyil Pratheeshkumar, Gang Chen, Zhuo Zhang, …
Toxicology and applied pharmacology, Vol.272(1), pp.108-116
10/01/2013
DOI: 10.1016/j.taap.2013.05.028
PMCID: PMC3823051
PMID: 23743303
url
https://doi.org/10.1016/j.taap.2013.05.028View
Published (Version of record) Open Access

Abstract

Environmental exposure to arsenic is known to cause various cancers. There are some potential relationships between cell malignant transformation and C-X-C chemokine receptor type 4 (CXCR4) expressions. Metastasis, one of the major characteristics of malignantly transformed cells, contributes to the high mortality of cells. CXCR4 and its natural chemokine ligand C-X-C motif ligand 12 (CXCL12) play a critical role in metastasis. Therefore, identification of nutritional factors which are able to inhibit CXCR4 is important for protection from environmental arsenic-induced carcinogenesis and for abolishing metastasis of malignantly transformed cells. The present study demonstrates that apigenin (4′,5,7-trihydroxyflavone), a natural dietary flavonoid, suppressed CXCR4 expression in arsenic-transformed Beas-2B cells (B-AsT) and several other types of transformed/cancer cells in a dose- and time-dependent manner. Neither proteasome nor lysosome inhibitor had any effect in reducing the apigenin-induced down-regulation of CXCR4, indicating that apigenin-induced down-regulation of CXCR4 is not due to proteolytic degradation. The down-regulation of CXCR4 is mainly due to the inhibition of nuclear factor κB (NF-κB) transcriptional activity. Apigenin also abolished migration and invasion of transformed cells induced by CXCL12. In a xenograft mouse model, apigenin down-regulated CXCR4 expression and suppressed tumor growth. Taken together, our results show that apigenin is a novel inhibitor of CXCR4 expression. This dietary flavonoid has the potential to suppress migration and invasion of transformed cells and prevent environmental arsenic-induced carcinogenesis. •Apigenin has a potential in preventing environmental arsenic induced carcinogenesis.•Apigenin suppresses CXCR4 in malignant transformed cells in vitro and in vivo.•The down-regulation of CXCR4 is mainly due to inhibition of NF-κB activity.
Apigenin CXCL12 CXCR4 Metastasis Transformed cell

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