Activation of PPARγ inhibits cell growth and induces apoptosis in human gastric cancer cells

AbstractWe investigated the expression of peroxisome proliferator-activated receptor γ (PPARγ) and the role of PPARγ in cell growth in human gastric cancer cells. Reverse transcription-polymerase chain reaction, Northern blot and Western blot analyses showed that a human gastric cancer cell line, MKN45, expressed PPARγ mRNA and protein. Luciferase assay in MKN45 cells showed that troglitazone, a selective ligand for PPARγ, transactivated the transcription of a peroxisome proliferator response element-driven promoter. Troglitazone or pioglitazone, selective ligands for PPARγ, inhibited the growth of MKN45 cells in a dose-dependent manner. Co-incubation of MKN45 cells with troglitazone induced DNA ladder formation. These results suggest that human gastric cancer cells express PPARγ and that activation of PPARγ inhibits cell growth and induces apoptosis in gastric cancer cells

Octreotide-Treated Diabetes Accompanied by Endogenous Hyperinsulinemic Hypoglycemia and Protein-Losing Gastroenteropathy

Occurrence of hypoglycemia in diabetes patients is very rare. We report here a case of frequent hypoglycemic attacks caused by inappropriate endogenous hyperinsulinemia in a female patient with poorly controlled diabetes and protein-losing gastroenteropathy. The blood glucose profiles of the patient were unstable. Results of the fasting test performed to investigate the cause of hypoglycemia suggested endogenous hyperinsulinism. Repeated selective arterial calcium injection tests suggested that hyperinsulinemia might be extrapancreatic in origin. However, efforts to detect a responsible lesion such as insulinoma were unsuccessful. Octreotide was used for the treatment of hypoglycemia and protein-losing gastroenteropathy. After treatment, although her leg edema caused by hypoalbuminemia persisted, hypoglycemia almost disappeared

Octreotide-Treated Diabetes Accompanied by Endogenous Hyperinsulinemic Hypoglycemia and Protein-Losing Gastroenteropathy

Occurrence of hypoglycemia in diabetes patients is very rare. We report here a case of frequent hypoglycemic attacks caused by inappropriate endogenous hyperinsulinemia in a female patient with poorly controlled diabetes and protein-losing gastroenteropathy. The blood glucose profiles of the patient were unstable. Results of the fasting test performed to investigate the cause of hypoglycemia suggested endogenous hyperinsulinism. Repeated selective arterial calcium injection tests suggested that hyperinsulinemia might be extrapancreatic in origin. However, efforts to detect a responsible lesion such as insulinoma were unsuccessful. Octreotide was used for the treatment of hypoglycemia and protein-losing gastroenteropathy. After treatment, although her leg edema caused by hypoalbuminemia persisted, hypoglycemia almost disappeared

Thiazolidinediones enhance vascular endothelial growth factor expression and induce cell growth inhibition in non-small-cell lung cancer cells

<p>Abstract</p> <p>Background</p> <p>It is known that thiazolidinediones are involved in regulating the expression of various genes, including the vascular endothelial growth factor (VEGF) gene via peroxisome proliferator-activated receptor γ (PPARγ); VEGF is a prognostic biomarker for non-small-cell lung cancer (NSCLC).</p> <p>Methods</p> <p>In this study, we investigated the effects of troglitazone and ciglitazone on the mRNA expression of VEGF and its receptors in human NSCLC cell lines, RERF-LC-AI, SK-MES-1, PC-14, and A549. These mRNA expressions were evaluated by quantitative real-time reverse transcription-polymerase chain reaction (RT-PCR) analysis. We also studied the effect of Je-11, a VEGF inhibitor, on the growth of these cells.</p> <p>Results</p> <p>In NSCLC cells, thiazolidinediones increased the mRNA expression of VEGF and neuropilin-1, but not that of other receptors such as fms-like tyrosine kinase and kinase insert domain receptor-1. Furthermore, the PPARγ antagonist GW9662 completely reversed this thiazolidinedione-induced increase in VEGF expression. Furthermore, the addition of VEGF inhibitors into the culture medium resulted in the reversal of thiazolidinedione-induced growth inhibition.</p> <p>Conclusions</p> <p>Our results indicated that thiazolidinediones enhance VEGF and neuropilin-1 expression and induce the inhibition of cell growth. We propose the existence of a pathway for arresting cell growth that involves the interaction of thiazolidinedione-induced VEGF and neuropilin-1 in NSCLC.</p

Involvement of MEK-ERK signaling pathway in the inhibition of cell growth by troglitazone in human pancreatic cancer cells

Elsevier Inc., Wataru Motomura, Satoshi Tanno, Nobuhiko Takahashi, Miho Nagamine, Mitsuko Fukuda (Sawamukai), Yutaka Kohgo and Toshikatsu Okumura, BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 332(1), 2005, 89-94. authorIn the present study, we examined a role of mitogen-activated protein kinases (MAPKs), extracellular signal releted kinase (ERK), c-Jun N-terminal protein kinase (JNK) and p38 MAPK in troglitazone-induced inhibition of cell growth in human pancreatic cancer cells. Among the three kinases, troglitazone specifically inhibited the phosphorylation of ERK1/2 in a dose- and time-dependent manner. Troglitazone also down-regulated the protein expression of mitogen-activated protein kinase kinase (MEK)1/2, an upstream molecule that regulates ERK phosphorylation. Treatment of human pancreatic cancer cells with specific MEK inhibitor, PD98059 or U0126 inhibited ERK1/2 phosphorylation and cell growth. These results suggest for the first time that the inhibition of the MEK1/2-ERK1/2 signaling pathway may be implicated in the growth inhibitory effect by troglitazone in human pancreatic cancer cells

Up-regulation of ADRP in fatty liver in human and liver steatosis in mice fed with high fat diet

Elsevier Inc., Wataru Motomura, Mitsutaka Inoue, Takaaki Ohtake, Nubuhiko Takahashi, Miho Nagamine, Satoshi Tanno, Yutaka Kohgo and Toshikatsu Okumura, Biochemical and Biophysical Research Communications , 340(4), 2006, 1111-1118. authorThe present study was performed to examine a role of adipose differentiation-related protein (ADRP) in the process of liver steatosis. Immunohistochemical findings indicated that ADRP protein expression is increased in the hepatocytes in patients with fatty liver when compared with normal liver. ADRP protein expression is localized in the surface of lipid droplets in the hepatocytes. Increased expression of ADRP mRNA and protein was similarly observed in fatty liver in ob/ob mice and the liver steatosis induced by high fat diet in mice. The up-regulation of ADRP mRNA and protein in the liver by high fat diet was identified in the surface of lipid droplets in a time dependent manner. Recent studies demonstrated that up-regulation of PPARg in the hepatocytes is deeply involved in liver steatosis. To clarify whether ADRP expression is increased by PPARg activation in hepatocytes, we examined the effect of a PPARg ligand, troglitazone, on ADRP mRNA expression in HepG2 cells. ADRP mRNA expression was increased by troglitazone in dose and time dependent manners. All these results suggest that ADRP is up-regulated in liver steatosis in human and mice and that high fat diet increases expression of ADRP through PPARg activation, followed by induction of liver steatosis

WP-106: Mobile-based Streaming System of Spatial Audiovisual Contents and Web-based Design System

<p>WP-106: Mobile-based Streaming System of Spatial Audiovisual Contents and Web-based Design System</p