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carcinogenesis/phosphatase
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The role of T-cell protein tyrosine phosphatase in epithelial carcinogenesis.
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T-cell protein tyrosine phosphatase (TC-PTP, encoded by PTPN2) is a nonreceptor PTP that is most highly expressed in hematopoietic tissues. TC-PTP modulates a variety of physiological functions including cell cycle progression, cell survival and proliferation, and hematopoiesis through tyrosine
Down-regulation of dual-specificity phosphatase 5 in gastric cancer by promoter CpG island hypermethylation and its potential role in carcinogenesis.
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Dual-specificity phosphatase 5 (DUSP5), which regulates the duration and magnitude of ERK1/2 phosphoactivation within the mitogen-activated protein kinase (MAPK) cascade, has recently been proposed to be a tumor suppressor. However, the epigenetic regulation of DUSP5 and its critical roles in
Nodularin, a potent inhibitor of protein phosphatases 1 and 2A, is a new environmental carcinogen in male F344 rat liver.
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Nodularin and microcystin-LR are cyanobacterial toxins and environmental hazards. Nodularin inhibits protein phosphatases 1 and 2A with the same potency as does microcystin-LR, which has recently been identified as a potent tumor promoter in rat liver. Our results suggested that nodularin is also a
Demonstration of glucose-6-phosphatase and peroxisomal catalase activity by ultrastructural cytochemistry in oval cells from livers of carcinogen-treated rats.
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Oval cells isolated from livers of carcinogen-treated rats have morphologic and biochemical features of immature hepatocytes but seem to lack glucose-6-phosphatase (G6Pase) activity. The authors reinvestigated this question using histochemical methods for visualization of G6Pase activity by light
Loss of protein phosphatase 6 in mouse keratinocytes increases susceptibility to ultraviolet-B-induced carcinogenesis.
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We previously reported that deficiency in the gene encoding the catalytic subunit of protein phosphatase 6 (Ppp6c) predisposes mouse skin tissue to papilloma formation initiated by DMBA. Here, we demonstrate that Ppp6c loss acts as a tumor promoter in UVB-induced squamous cell carcinogenesis.
Effects of the hepatocarcinogenic peroxisome-proliferating hypolipidemic agents clofibrate and nafenopin on the rat liver cell membrane enzymes gamma-glutamyltranspeptidase and alkaline phosphatase and on the early stages of liver carcinogenesis.
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The effects of the hepatocarcinogenic peroxisome proliferating hypolipidemic agents clofibrate (CF) and nafenopin (NF) on rat liver carcinogenesis initiated by N-2-fluorenylacetamide (FAA) were studied and compared with that of the neoplasm promoter phenobarbital (PB). Male F344 rats were fed 0.02%
A yeast homologue of the human phosphotyrosyl phosphatase activator PTPA is implicated in protection against oxidative DNA damage induced by the model carcinogen 4-nitroquinoline 1-oxide.
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The model carcinogen 4-nitroquinoline 1-oxide (4-NQO) has historically been characterized as "UV-mimetic" with respect to its genotoxic properties. However, recent evidence indicates that 4-NQO, unlike 254-nm UV light, may exert significant cytotoxic and/or mutagenic potential via the generation of
Phosphorylation of protein phosphatase 2A facilitated an early stage of chemical carcinogenesis.
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Protein phosphatase 2A (PP2A) is a serine-threonine phosphatase that regulates cell signaling pathways. Its inactivation is correlated with tumor malignancy, possibly due to the effects on cell differentiation and malignant cell transformation. Therefore, it has been noted that PP2A could be a
Role of PTEN, a lipid phosphatase upstream effector of protein kinase B, in epithelial thyroid carcinogenesis.
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Both benign and malignant thyroid disease are well-established components of Cowden syndrome (CS), an autosomal dominant disorder characterized by multiple hamartomas and breast cancer that may be considered a phakomatosis. The susceptibility gene for CS is PTEN, a tumor suppressor gene on 10q23.3
Alterations in receptor-mediated kinases and phosphatases during carcinogenesis.
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Increased phosphorylation in cancers can stimulate growth and up-regulate certain receptors. To test whether the functional response of phosphatase receptors is up-regulated during carcinogenesis, we examined the effects of ligands on net phosphorylation in isolated membranes derived from hamster
Chemical carcinogenesis in the hamster cheek pouch. Influence of inhibitors and inducers of alkaline phosphatase.
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Squamous cell carcinomas were induced in the hamster cheek pouch with 9,10-dimethyl-1,2-benzanthracene. The process of carcinogenesis was inhibited by phenylphosphate, an inducer of alkaline phosphatase. Orthophosphate and l-phenylalanine, which inhibit alkaline phosphatase, had a promoting effect
Detection of mutagens-carcinogens: carcinogen-induced lesions pinpointed by alkaline phosphatase activity in fixed gastric specimens from rats.
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Alkaline phosphatase (AP) activity was not detectable by histochemical staining in the glandular stomachs of normal rats. However, AP activity was present at high levels in the brush borders of the intestine and persisted after fixation of the tissues in Formalin at room temperature. Foci of AP
Expression of mitogen-activated protein kinase phosphatase-1 in the early phases of human epithelial carcinogenesis.
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Many mitogens and human oncogenes activate extracellular regulated kinases (ERKs), which in turn convey proliferation signals. ERKs or mitogen-activated protein (MAP) kinases are inactivated in vitro by MAP kinase phosphatases (MKPs). The gene encoding one of these MKPs, MKP-1, is a serum-inducible
The tyrosine phosphatase PTPRJ/DEP-1 genotype affects thyroid carcinogenesis.
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We recently isolated the r-PTPeta gene, which encodes a receptor-type tyrosine phosphatase protein that suppresses the neoplastic phenotype of retrovirally transformed rat thyroid cells. The human homologue gene PTPRJ/DEP-1 is deleted in various tumors. Moreover, the Gln276Pro polymorphism, located
Is NEDD4-1 a negative regulator of phosphatase and tensin homolog in gastric carcinogenesis?
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The expression of phosphatase and tensin homolog (PTEN), a tumor suppressor gene, is frequently down-regulated in gastric carcinomas due to mutation, loss of heterozygosity, and promoter hypermethylation. However, it is unknown if additional mechanisms may account for the down-regulation of PTEN
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