Curcumin inhibits cell proliferation and promotes apoptosis of laryngeal cancer cells through Bcl-2 and PI3K/Akt, and by upregulating miR-15a

Curcumin is a natural compound extracted from the dried rhizomes of (curcuma root or zedoary) that exhibits extensive pharmacological effects and low toxicity. The aim of the present study was to investigate whether curcumin inhibits cell proliferation and promotes apoptosis of laryngeal cancer thro...

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Bibliographic Details
Published in:Oncology letters 2017-10, Vol.14 (4), p.4937-4942
Main Authors: Mou, Shaofeng, Zhou, Zhongxin, He, Yukai, Liu, Fuxing, Gong, Lili
Format: Article
Language:English
Subjects:
Air pollution
Apoptosis
Biotechnology
Cancer therapies
Cell growth
Kinases
Laryngeal cancer
Medical prognosis
Metabolism
Mortality
Oncology
Protein expression
Proteins
Signal transduction
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Summary:Curcumin is a natural compound extracted from the dried rhizomes of (curcuma root or zedoary) that exhibits extensive pharmacological effects and low toxicity. The aim of the present study was to investigate whether curcumin inhibits cell proliferation and promotes apoptosis of laryngeal cancer through Bcl-2 and phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt), and by upregulating microRNA-15a (miR-15a). It was demonstrated that curcumin inhibits cell proliferation, and promotes apoptosis and increased caspase-3 activity of human laryngeal cancer cells. Furthermore, curcumin decreased Bcl-2 and PI3K protein expression, and decreased the phospho (p)-Akt protein expression of human laryngeal cancer cells. Furthermore, curcumin activated miR-15a expression by human laryngeal cancer cells. Suppression of miR-15a expression reversed the anticancer effect of curcumin on cell proliferation of human laryngeal cancer cells and increased Bcl-2 and PI3K/Akt protein expression in AMC-HN-8 cells treated with 40 µM of curcumin. The results of the present study suggest that curcumin inhibits cell proliferation and promotes apoptosis of laryngeal cancer cells through Bcl-2 and PI3K/Akt, and by upregulating miR-15a.
ISSN:1792-1074
1792-1082
DOI:10.3892/ol.2017.6739