4.7 Article

Lycopene suppresses gastric cancer cell growth without affecting normal gastric epithelial cells

Journal

JOURNAL OF NUTRITIONAL BIOCHEMISTRY
Volume 116, Issue -, Pages -

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/j.jnutbio.2023.109313

Keywords

apoptosis; bioinformatics analysis; cell cycle; gastric cancer; lycopene

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Lycopene, a natural carotenoid, inhibits the growth and induces apoptosis in gastric cancer cells. It decreases CCNE1 expression and increases the levels of TP53, making it a potential target therapy reagent for gastric cancer.
Gastric cancer is one of the leading causes of cancer-related death worldwide. Lycopene, a natural carotenoid, has potent antioxidant activity and anti-cancer effects against several types of cancers. However, the mechanism for the anti-gastric cancer effects of lycopene remains to be fully clarified. Normal gastric epithelial cell line GES-1 and gastric cancer cell line AGS, SGC-7901, Hs746T cells were treated with different concentrations of lycopene and the effects of lycopene were compared. Lycopene specifically suppressed cell growth monitored by Real-Time Cell Analyzer, induced cell cycle arrest and cell apoptosis detected by flow cytometry, and lowered mitochondrial membrane potentials assessed by JC-1 staining of AGS and SGC-7901 cells, while did not affect those of GES-1 cells. Lycopene did not affect the cell growth of Hs746T cells harboring TP53 mutation. Further bioinformatics analysis predicted 57 genes with up-regulated expression levels in gastric cancer and decreased function in cells after lycopene treatment. Quantitative PCR and Western Blot were used to check the critical factors in the cell cycle and apoptosis signaling pathway. Lycopene decreased the high expression levels of CCNE1 and increased the levels of TP53 in AGS and SGC-7901 cells without affecting those in GES-1 cells. In summary, lycopene could effectively suppress gastric cancer cells with CCNE1-amplification, which could be a promising target therapy reagent for gastric cancer. (c) 2023 Elsevier Inc. All rights reserved.

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