Inhibition of IGF-1 signaling by genistein: modulation of E-cadherin expression and downregulation of β-catenin signaling in hormone refractory PC-3 prostate cancer cells.

Elevated levels of insulin-like growth factor-1 (IGF-1) are associated with an increased risk of several different cancers, including prostate cancer. Inhibition of IGF-1 and the downstream signaling pathways mediated by the activation of the IGF-1 receptor (IGF-1R) may be involved in inhibiting prostate carcinogenesis. We investigated whether genistein downregulated the IGF-1/IGF-1R signaling pathway and inhibited cell growth in hormone refractory PC-3 prostate cancer cells.

Protective effect of lycopene on oxidative stress-induced cell death of pancreatic acinar cells.

Previously we showed that the underlying mechanism of oxidative stress-induced apoptosis is nuclear loss of DNA repair protein Ku70 and Ku80, which are involved in the DNA repair process of double-strand breaks. Lycopene acts as an antioxidant and a singlet oxygen quencher. In the present study, we aim to investigate whether lycopene protects oxidative stress-induced cell death of pancreatic acinar AR42J cells by preventing the loss of Ku70 in the nucleus.

15-Deoxy-delta 12, 14,-prostaglandin J2 suppresses nuclear factor-kappaB-mediated apoptosis of Helicobacter pylori-infected gastric epithelial cells.

Helicobacter pylori deregulates the genes that control homeostasis between apoptosis and cell proliferation of gastric epithelial cells. Nuclear factor-kappaB (NF-kappaB) has an important role in H. pylori-induced apoptosis in gastric epithelial cells.

Mechanism of alpha-lipoic acid-induced apoptosis of lung cancer cells.

Alpha-lipoic acid (LA) shows a protective effect on oxidative stress-induced apoptosis while it induces apoptosis in various cancer cells. Intracellular Ca(2+) plays a central role in triggering apoptotic pathways. In the present study, we aim to investigate whether LA induces apoptosis in lung cancer cells and whether Ca(2+) is involved in LA-induced apoptosis.

A combination of soy isoflavone supplementation and exercise improves lipid profiles and protects antioxidant defense-systems against exercise-induced oxidative stress in ovariectomized rats.

Menopause is often accompanied with weight gain, metabolic lipid abnormalities, and oxidative stress. In this study, we investigated the combined effects of exercise and soy isoflavone supplementation on the lipid profiles and antioxidant capacities of ovariectomized rats. Twenty-five female Sprague-Dawley rats were divided into 5 groups: sham-operated, ovariectomized (OVX), OVX with exercise (OVX+EX), OVX with soy isoflavone supplementation (OVX+ISO), and OVX with both soy isoflavones and exercise (OVX+ISO+EX).

Inhibition of serine-threonine protein phosphatases in monocyte chemoattractant protein-1 expression in Helicobacter pylori-stimulated gastric epithelial cells.

The reversible phosphorylation of proteins controlled by protein kinases and protein phosphatases is a major mechanism that regulates a wide variety of cellular processes, such as inflammation. It has been reported that the activity of at least 30% of all proteins can be regulated by phosphorylation in eukaryotic cells. Among these proteins, mitogen-activated protein kinases (MAPK) and several transcription factors play pivotal roles in inflammation.

Role of vascular endothelial growth factor-D (VEGF-D) on IL-6 expression in cerulein-stimulated pancreatic acinar cells.

Cerulein pancreatitis is similar to human edematous pancreatitis with dysregulation of the digestive enzyme production and cytoplasmic vacuolization, the death of acinar cells, edema formation, and an infiltration of inflammatory cells into the pancreas. Our preliminary proteomic analysis showed increased expression of vascular endothelial growth factor-D (VEGF-D) in cerulein (10(-8)M)-treated pancreatic acinar cells. We hypothesized that VEGF-D may have a role in cerulein-induced cytokine expression in pancreatic acinar cells.