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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2010-9-27
pubmed:abstractText
Securin and ?-H2AX have been shown to regulate cell survival and genomic stability. However, it is still unknown how the expression and regulation of these proteins is altered following treatment with baicalein, a natural flavonoid extracted from the Scutellaria baicalensis root. In the present study, we investigate the possible roles of securin and ?-H2AX in baicalein-induced cancer cell death. Baicalein reduced cell viability in a variety of human cancer cell lines, including bladder, cervical, colon, and lung cancer cells. Interestingly, baicalein treatment (40-80?µM for 24 h) markedly inhibited securin expression, while the levels of ?-H2AX were elevated. Abnormal spindle formation and chromosomal segregation were induced by baicalein. Furthermore, wild type HCT116 cancer cells had a higher incidence of cytotoxicity and apoptosis than securin-null HCT116 cells following treatment with baicalein. In contrast, baicalein increased the levels of ?-H2AX to a similar extent in both cell types. Transfection with H2AX siRNA further increased baicalein-induced cell death. Additionally, blockade of the AKT pathway by treatment with wortmannin or AKT shRNA lowered the levels of ?-H2AX and enhanced cytotoxicity in baicalein-treated cells. Taken together, our findings suggest that the opposing effects of baicalein on securin and ?-H2AX levels may be involved in the regulation of cell viability and genomic stability by this compound.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1097-4644
pubmed:author
pubmed:copyrightInfo
© 2010 Wiley-Liss, Inc.
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
111
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
274-83
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Opposite expression of securin and ?-H2AX regulates baicalein-induced cancer cell death.
pubmed:affiliation
Molecular Anticancer Laboratory, Department of Biological Science and Technology, National Chiao Tung University, Hsinchu 30068, Taiwan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't