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

Suppressor T cell Inducing Factor from a Human Macrophage Like Cell Line-U 937

U 987, a human histiocytic lymphoma cell line, spontaneously produces a factor(M-SF) which inhibits blastogenic responses of lymphocytes and Interleukin 2(IL-2) activated killer(IAK) induction from human peripheral blood lymphocytes (PBL). We investigated the mechanism of the suppressor action and the physicochemical character of the M-SF. Suppressive activity of U 937 culture supernatant was absorbed with human peripheral blood T lymphocytes. When the M-SF pretreated T cells were added, the mitogenic response of fresh allogeneic or autologus PBL to phytohaemagglutinin(PHA), Concanavalin A(Con A) and pokeweed mitogen(PWM) were suppressed. In addition, IL-2 activated killer activity was suppressed when the M-SF pretreated T cells were present in the induction phase of IAK. These suppressions were mediated by soluble factors produced by M-SF treated T lymphocytes. These results suggest that the pretreatment of T lymphocytes with M-SF resulted in the induction of suppressor T lymphocytes. M-SF also inhibited the protein kinase activity associated with T cell membrane. The intensity of phosphorylated T cell membrane proteins with the molecular weights of 110, 94, 42, 38 and 34 killodaltons on SDS PAGE were decreased. Dephosphorylation of these proteins may be related to the functional alteration of T lymphocytes. CPG-10 Gel permeation and hydrophobic interaction column chromatographic analysis revealed that the M-SF was an extremely hydrophobic sialoprotein of which approximate molecular weight was 10,000 daltons

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