Please use this identifier to cite or link to this item: https://ir.swu.ac.th/jspui/handle/123456789/14042
ชื่อเรื่อง: Chrysin overcomes TRAIL resistance of cancer cells through Mcl-1 downregulation by inhibiting STAT3 phosphorylation
ผู้แต่ง: Lirdprapamongkol K.
Sakurai H.
Abdelhamed S.
Yokoyama S.
Athikomkulchai S.
Viriyaroj A.
Awale S.
Ruchirawat S.
Svasti J.
Saiki I.
Keywords: chrysin
cucurbitacin
glutathione
propolis
protein mcl 1
STAT3 protein
tumor necrosis factor related apoptosis inducing ligand
analysis
antineoplastic activity
apoptosis
article
cancer cell
cancer cell culture
cancer resistance
controlled study
down regulation
enzyme activation
enzyme inhibition
female
gene expression
HeLa cell
honeybee
human
human cell
immunoblotting
priority journal
protein phosphorylation
reverse transcription polymerase chain reaction
sensitization
signal transduction
uterine cervix cancer
Female
Flavonoids
Gene Expression Regulation, Neoplastic
Glutathione
HeLa Cells
Humans
Lung Neoplasms
Myeloid Cell Leukemia Sequence 1 Protein
NF-kappa B
Phosphorylation
Propolis
STAT3 Transcription Factor
TNF-Related Apoptosis-Inducing Ligand
Uterine Cervical Neoplasms
วันที่เผยแพร่: 2013
บทคัดย่อ: Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) selectively kills various types of cancer cells without harming normal cells, but TRAIL resistance has been frequently observed in cancer cells. Propolis (bee glue) is a material collected from various plants by honeybees and is a rich source of bioactive compounds, including the natural flavonoid chrysin, which possesses multiple anticancer effects. We investigated the mechanism underlying the TRAIL sensitization effect of chrysin, which is a major constituent of Thai propolis, in human lung and cervical cancer cell lines. Propolis extract and chrysin sensitizes A549 and HeLa human cancer cell lines to TRAIL-induced apoptosis. The TRAIL sensitization effect of chrysin is not mediated by inhibition of TRAIL-induced NF-κB activation or by glutathione depletion. Immunoblot analysis using a panel of anti-apoptotic proteins revealed that chrysin selectively decreases the levels of Mcl-1 protein, by downregulating Mcl-1 gene expression as determined by qRT-PCR. The contribution of Mcl-1 in TRAIL resistance was confirmed by si-Mcl-1 knockdown. Among signaling pathways that regulate Mcl-1 gene expression, only constitutive STAT3 phosphorylation was suppressed by chrysin. The proposed action of chrysin in TRAIL sensitization by inhibiting STAT3 and downregulating Mcl-1 was supported by using a STAT3-specific inhibitor, cucurbitacin-I, which decreased Mcl-1 levels and enhanced Key words: tumor necrosis factor-related apoptosis-inducing ligand, STAT3, apoptosis, propolis, natural products TRAIL-induced cell death, similar to that observed with chrysin treatment. In conclusion, we show the potential of chrysin in overcoming TRAIL resistance of cancer cells and elucidate its mechanism of action.
URI: https://ir.swu.ac.th/jspui/handle/123456789/14042
https://www.scopus.com/inward/record.uri?eid=2-s2.0-84879460546&doi=10.3892%2fijo.2013.1926&partnerID=40&md5=b3c88580e5076e8895199e6af1407c7b
ISSN: 10196439
Appears in Collections:Scopus 1983-2021

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