pituitrin and Carcinoma--Hepatocellular

Topics: Adrenergic beta-Antagonists; Ascites; Carcinoma, Hepatocellular; Catheterization; Diuretics; Hemorrhage; Hepatic Encephalopathy; Humans; Hypertension, Portal; Liver Cirrhosis; Liver Neoplasms; Nitroglycerin; Peritonitis; Somatostatin; Vasopressins

Topics: Animals; Carcinoma, Hepatocellular; Liver Neoplasms; Male; Rats; Rats, Wistar; Vasopressins

Intercellular signaling is highly coordinated in excitable tissues such as heart, but the organization of intercellular signaling in epithelia is less clear. We examined Ca(2+) signaling in hepatoma cells expressing the hepatocyte gap junction protein connexin32 (cx32) or the cardiac gap junction protein cx43, plus a fluorescently tagged V(1a) vasopressin receptor (V(1a)R). Release of inositol 1,4,5-trisphosphate (InsP(3)) in wild type cells increased Ca(2+) in the injected cell but not in neighboring cells, while the Ca(2+) signal spread to neighbors when gap junctions were expressed. Photorelease of caged Ca(2+) rather than InsP(3) resulted in a small increase in Ca(2+) that did not spread to neighbors with or without gap junctions. However, photorelease of Ca(2+) in cells stimulated with low concentrations of vasopressin resulted in a much larger increase in Ca(2+), which spread to neighbors via gap junctions. Cells expressing tagged V(1a)R similarly had increased sensitivity to vasopressin, and could signal to neighbors via gap junctions. Higher concentrations of vasopressin elicited Ca(2+) signals in all cells. In cx32 or cx43 but not in wild type cells, this signaling was synchronized and began in cells expressing the tagged V(1a)R. Thus, intercellular Ca(2+) signals in epithelia are organized by three factors: 1) InsP(3) must be generated in each cell to support a Ca(2+) signal in that cell; 2) gap junctions are necessary to synchronize Ca(2+) signals among cells; and 3) cells with relatively increased expression of hormone receptor will initiate Ca(2+) signals and thus serve as pacemakers for their neighbors. Together, these factors may allow epithelia to act in an integrated, organ-level fashion rather than as a collection of isolated cells.

Topics: Animals; Calcium Signaling; Carcinoma, Hepatocellular; CHO Cells; Connexin 43; Connexins; Cricetinae; Epithelial Cells; Gap Junction beta-1 Protein; Gap Junctions; Intercellular Junctions; Kinetics; Recombinant Fusion Proteins; Reverse Transcriptase Polymerase Chain Reaction; Signal Transduction; Tumor Cells, Cultured; Vasopressins

Topics: Arteriovenous Fistula; Blood Component Transfusion; Blood Transfusion; Carcinoma, Hepatocellular; Child; Endoscopy, Gastrointestinal; Epistaxis; Esophageal and Gastric Varices; Female; Gastrointestinal Hemorrhage; Hematemesis; Hepatic Artery; Humans; Hypertension, Portal; Liver Neoplasms; Portal Vein; Sclerotherapy; Tomography, X-Ray Computed; Ultrasonography; Vasopressins

Teleocidin, a phorbol ester-type tumor promoter, inhibits cell proliferation and calcium mobilization induced by epidermal growth factor and vasopressin in PLC/PRF/5 hepatoma cells. These inhibitory effects of teleocidin were observed even after a prolonged exposure of the hepatoma cells to this promoter, suggesting the presence of down-regulation-resistant protein kinase C in this hepatoma cell line. Column chromatography of cytosolic fractions showed three separate peaks of protein kinase C activity, two being down-regulation-sensitive while one was down-regulation-resistant. This down-regulation-resistant PKC is suggested to be responsible for the inhibitory effect of teleocidin on cell proliferation and calcium mobilization induced by epidermal growth factor and vasopressin.

Topics: Calcium; Carcinoma, Hepatocellular; Cell Count; Cell Division; Cell Line; Down-Regulation; Epidermal Growth Factor; Humans; Lyngbya Toxins; Protein Kinase C; Tumor Cells, Cultured; Vasopressins

Among the malignant tumors of nonendocrine origin that are capable of producing polypeptide hormones and of manifesting as different endocrine syndromes discussed here are ectopic ACTH syndrome, SIADH, and ectopic gonadotropin-producing tumors.

Topics: Adrenocorticotropic Hormone; Carcinoma, Hepatocellular; Carcinoma, Small Cell; Chorionic Gonadotropin; Cushing Syndrome; Diagnosis, Differential; Erythropoietin; Follicle Stimulating Hormone; Gynecomastia; Hormones, Ectopic; Humans; Hyperthyroidism; Hypoglycemia; Hyponatremia; Liver Neoplasms; Lung Neoplasms; Luteinizing Hormone; Male; Paraneoplastic Endocrine Syndromes; Polycythemia; Puberty, Precocious; Thyrotropin; Vasopressins; Water Intoxication

Ectopic production of polypeptide hormones by tumors of nonendocrine tissues can serve as a clue to diagnosis of the tumor and as a focus for management of the patient with cancer. In the differential diagnosis of syndromes of endocrine hyperfunction, the ectopic hormone syndromes have achieved an increasingly prominent position. Available evidence on the properties of ectopic ACTH, MSH, parathyroid hormone, erythropoietin, gonadotropins, and thyrotropin is consistent with the unifying hypothesis of genetic derepression.

Topics: Abdominal Neoplasms; Adenocarcinoma; Adrenocortical Hyperfunction; Brain Neoplasms; Carcinoma, Bronchogenic; Carcinoma, Hepatocellular; Carcinoma, Small Cell; Cysts; Diagnosis, Differential; Fibroma; Hemangiosarcoma; Humans; Hyperparathyroidism; Hypoglycemia; Kidney Diseases; Kidney Neoplasms; Liver Neoplasms; Lung Neoplasms; Paraneoplastic Endocrine Syndromes; Pheochromocytoma; Polycythemia; Sarcoma; Thoracic Neoplasms; Vasopressins

Topics: 5-Hydroxytryptophan; Carcinoid Tumor; Carcinoma, Hepatocellular; Carotid Body Tumor; Catecholamines; Cushing Syndrome; Endocrine System Diseases; Female; Fibrosarcoma; Humans; Hyperthyroidism; Hypoglycemia; Hyponatremia; Liver Neoplasms; Lung Neoplasms; Male; Neoplasms; Polycythemia Vera; Puberty, Precocious; Vasopressins