Anticancer Effect of Lycopene in Gastric Carcinogenesis

Abstract

Gastric cancer ranks as the most common cancer and the second leading cause of cancer-related death in the world. Risk factors of gastric carcinogenesis include oxidative stress, DNA damage, Helicobacter pylori infection, bad eating habits, and smoking. Since oxidative stress is related to DNA damage, smoking, and H. pylori infection, scavenging of reactive oxygen species may be beneficial for prevention of gastric carcinogenesis. Lycopene, one of the naturally occurring carotenoids, has unique structural and chemical features that contributes to a potent antioxidant activity. It shows a potential anticancer activity and reduces gastric cancer incidence. This review will summarize anticancer effect and mechanism of lycopene on gastric carcinogenesis based on the recent experimental and clinical studies.

Keywords: Anticancer effect; Gastric carcinogenesis; Lycopene.

Figure 1.

A schematic overview of the protective effect of lycopene against gastric carcinogenesis. Smoking, inflammation, and Helicobacter pylori infection induce oxidative stress which leads to DNA damage, ERK activation and p53 overexpression, decreased activities of antioxidant enzymes (GSH, GST, GPx) as well as impaired immune function. Low activities of antioxidant enzymes may decrease immune function of gastric mucosa. ERK activation and p53 overexpression induce cell cycle disturbances and inhibition of apoptosis as well as hyper-proliferation, resulting in gastric carcinogenesis. Poor diet, bad eating habits, and family history may be risk factors to induce DNA damage and cell cycle disturbances by affecting intrinsic factors or producing reactive oxygen species or oncogenic factors. Lycopene scavenges reactive oxygen species and stimulates activities of antioxidant enzymes, which protects gastric mucosa against oxidative stress-induced ERK activation, p53 induction, cell cycle disturbances, and impaired immune function. Therefore, lycopene may prevent oxidative stress-mediated gastric carcinogenesis. ERK, extracellular signal-regulated kinase; GSH, glutathione; GST, glutathione-S-transferase; GPx, glutathione peroxidase.