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

摘要: Abstract Environmental exposure to arsenic is known 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 malignantly transformed cells, contributes high mortality cells. CXCR4 its natural ligand motif 12 (CXCL12) play a critical role in metastasis. Therefore, identification nutritional factors which able inhibit important for protection from environmental arsenic-induced carcinogenesis abolishing metastasis The present study demonstrates that apigenin (4′,5,7-trihydroxyflavone), dietary flavonoid, suppressed expression arsenic-transformed Beas-2B cells (B-AsT) several other types transformed/cancer dose- time-dependent manner. Neither proteasome nor lysosome inhibitor had any effect reducing apigenin-induced down-regulation CXCR4, indicating not due proteolytic degradation. mainly inhibition nuclear factor κB (NF-κB) transcriptional activity. Apigenin also abolished migration invasion induced by CXCL12. In xenograft mouse model, down-regulated tumor growth. Taken together, our results show novel expression. This flavonoid has suppress prevent carcinogenesis.