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Comparison of Cell Growth Inhibition by Various Phenolic‐enriched Sorghum Accessions in Human Liver Carcinoma HepG2 Cells
Author(s) -
Chen Xi,
Rhodes Davina,
Herald Tom,
Su Xiaoyu,
Xu Jingwen,
Shen Yanting,
Wang Weiqun
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.974.6
Subject(s) - cell growth , apoptosis , growth inhibition , sorghum , cell , cytotoxicity , liver cancer , cancer cell , cell cycle , hepatocellular carcinoma , chemistry , cancer , biology , food science , cancer research , biochemistry , agronomy , in vitro , genetics
Phenolic agents in plant foods have been associated with chronic disease prevention, especially cancer. In this study, we selected 13 phenolic‐enriched sorghum accessions and tested their extracted phenolic agents on cell growth inhibition in human hepatocellular carcinoma HepG2 cells. Total phenolic contents as determined by Folin‐Ciocalteu were 30–64 mg GAE/g DW on the extracts of various accessions. Treatment of HepG2 cells with the extracted phenolics at 0–200 uM up to 72 hrs resulted in a dose‐ and time‐dependent reduction in cell number. IC 50 was varied from 85 to 221 ug/mL for each of the 13 extracted accessions when compared with a negative control at 1,275 ug/mL. Furthermore, the underlying mechanism of cell growth inhibition was examined in one accession, indicating the cell growth inhibition that appeared not to be mediated by cytotoxicity, but cytostatic mechanism with a dose‐dependent increase of cell cycle arrest at G2/M. Meanwhile, the percentage of apoptotic cells were significantly induced. Our on‐going studies conducted on the colon cancer cells will be compared with these liver cancer cell data for a better understanding of anti‐cancer cell activities by sorghum phenolic agents (supported by USDA Cooperative Award 58‐3020‐5‐016). Support or Funding Information supported by USDA Cooperative Award 58‐3020‐5‐016