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Galangin‐induced cell arrest and apoptosis of nasopharyngeal carcinoma cells through suppression of PI3K/Akt signaling pathway
Author(s) -
Lee ChuanChun,
Lin MengLiang,
Meng MengHsiao,
Chen ShihShun
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.1108.10
Subject(s) - galangin , protein kinase b , pi3k/akt/mtor pathway , chemistry , kinase , apoptosis , microbiology and biotechnology , cell cycle checkpoint , nasopharyngeal carcinoma , autophosphorylation , cancer research , protein kinase a , biology , cell cycle , biochemistry , medicine , kaempferol , radiation therapy , antioxidant , quercetin
Aberrant activation of phosphatidylinositol 3‐kinase (PI3K)–(protein kinase B) Akt signaling is associated with nasopharyngeal carcinoma (NPC) cells resistance to conventional chemo / radiotherapy. We show that natural active compound 3, 5, 7‐trihydroxyflavone (galangin), a type of bioflavonoid extracted from the galangal root ( Alpinia galangal ), can induce apoptosis and S‐phase arrest of NPC cells through p53‐medulated expression of Bax and p21. Using cell cycle synchronization techniques, we demonstrated that S‐phase synchronized NPC cells were more sensitive to galangin‐induced apoptosis. In ATP‐competitive inhibition assay and thin‐layer chromatography separation of the γ‐ 32 P‐labeled phosphatidylinositol 3, 4, 5‐triphosphate product of kinase reaction with purified recombinant p85α and p110α proteins, we found that galangin might be an ATP‐competitive inhibitor by competing ATP binding site on PI3K catalytic subunit p110 alpha with ATP. Our results indicate that galangin induces p53‐mediated cell cycle arrest and apoptosis of NPC cells by interaction with ATP binding site on p110 alpha catalytic domain of PI3K. Support or Funding Information