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Resveratrol‐Mediated Repression of a Liver Cancer Cell Line
Author(s) -
Zhang Baochun,
Lakshmanan Jaganathan,
Motameni Amirreza,
Harbrecht Brian G
Publication year - 2017
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.31.1_supplement.1067.5
Subject(s) - resveratrol , viability assay , apoptosis , cell growth , cell , microbiology and biotechnology , bromodeoxyuridine , chemistry , programmed cell death , andrology , biology , biochemistry , medicine
Among the polyphenols, resveratrol ( trans‐ 3,5,4′‐trihydroxystilbene) is a natural product with potential for the treatment of several diseases, including cancer. The aim of present study was to investigate the ability of resveratrol (RES) to inhibit HepG2 liver cancer cell growth, and examined the underlying mechanisms. HepG2 cells were cultured in MEM with 5% FBS, the cells were treated with vehicle, 50 micro Molar, or 100 micro Molar of RES for 48 hours. Cell viability measured by MTT ((3‐(4,5‐Dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide) stain were decreased approximately 26% and 32% respectively among the cells treated with RES. To understand whether RES – induced cell death and/or cell proliferation contributed the loss of cell viability, Bromodeoxyuridine (BrDU) and apoptosis gene screen assay were performed. HepG2 cells treated with 50 micro Molar and 100 micro Molar RES exhibited a marked decrease in BrDU incorporation rate (18% and 5%); indicating that suppressed cell proliferation played a major role of the effects of RES on HepG2 cell viability. Multi‐Target apoptosis paths scan showed that 100 micro Molar RES induced a significantly increase of both phosphorylated‐ and total‐p53 protein level. Meanwhile, no significant changes were observed on level of dephosphorylated and total Bad, cleaved caspase 3, and cleaved PARP on cells treated with RES. In this study, we found that RES induced inhibition of HepG2 cell viability by suppressing their proliferation. Increased phosphorylation of p53 may contribute the effect of RES and may trigger apoptosis at long time. Thus, these findings suggest that RES has potential as a candidate agent against human liver cancer.