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Oxid Med Cell Longev. 2017;2017:1379430. doi: 10.1155/2017/1379430. Epub 2017 Jan 22.

Synthetic Isoliquiritigenin Inhibits Human Tongue Squamous Carcinoma Cells through Its Antioxidant Mechanism.

Author information

1
School of Basic Medical Sciences, Lanzhou University, Lanzhou, Gansu Province 730000, China; Key Lab of Preclinical Study for New Drugs of Gansu Province, Lanzhou, Gansu Province 730000, China; Department of Physiology and Pathophysiology, Fudan University Shanghai Medical College, Shanghai 200000, China.
2
School of Basic Medical Sciences, Lanzhou University, Lanzhou, Gansu Province 730000, China; Key Lab of Preclinical Study for New Drugs of Gansu Province, Lanzhou, Gansu Province 730000, China.
3
Jining Medical University, Jining, Shandong Province 272067, China.
4
Northwest Nationalities University Hospital, Lanzhou, Gansu Province 730000, China.
5
School of Public Health, Curtin University, Centre for Genetic Origins of Health and Disease, The University of Western Australia and Curtin University, M409, 35 Stirling Highway, Crawley, WA 6009, Australia.

Abstract

Isoliquiritigenin (ISL), a natural antioxidant, has antitumor activity in different types of cancer cells. However the antitumor effect of ISL on human tongue squamous carcinoma cells (TSCC) is not clear. Here we aimed to investigate the effects of synthetic isoliquiritigenin (S-ISL) on TSCC and elucidate the underlying mechanisms. S-ISL was synthesized and elucidated from its nuclear magnetic resonance spectrum and examined using high performance liquid chromatography. The effects of S-ISL on TSCC cells (Tca8113) were evaluated in relation to cell proliferation, apoptosis and adhesion, migration, and invasion using sulforhodamine B assay, fluorescence microscopy technique, flow cytometry (FCM) analysis, and Boyden chamber assay. The associated regulatory mechanisms were examined using FCM and fluorescence microscopy for intracellular reactive oxygen species (ROS) generation, Gelatin zymography assay for matrix metalloproteinase (MMP) activities, and Western blot for apoptosis regulatory proteins (Bcl-2 and Bax). Our data indicated that S-ISL inhibited Tca8113 cell proliferation, adhesion, migration, and invasion while promoting the cell apoptosis. Such effects were accompanied by downregulation of Bcl-2 and upregulation of Bax, reduction of MMP-2 and MMP-9 activities, and decreased ROS production. We conclude that S-ISL is a promising agent targeting TSCC through multiple anticancer effects, regulated by its antioxidant mechanism.

PMID:
28203317
PMCID:
PMC5292127
DOI:
10.1155/2017/1379430
[Indexed for MEDLINE]
Free PMC Article

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