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Query: UNIPROT:P00750 (PLA)
 16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This recent study describes the growth characteristics of ACR skin fibroblasts in culture and their differential susceptibility to transformation by Kirsten murine sarcoma virus (Ki-MSV). The SF were derived from normal appearing subepidermoid biopsies of ACR individuals, their progeny and ocntrols. Normal SF were contact-inhibited and grew only in 15% FCS. SF of ACR subjects, and some asymptomatic ACR progeny were not contact inhibited, grew in both 1% and 15% FCS and were considerably more susceptible to transformation by Ki-MSV than were control SF. The virally transformed SF showed a loss of anchorage dependency in methylcellulose and formed tumors in athymic mice. The results suggest the presence of early and previously undetected metabolic lesions in SF from clinically asymptomatic subjects. These phenotype markers are currently evaluated for their utility in the clinical diagnosis of individuals with latent ACR and those at increased risk for colon cancer. SF from ACR individuals have been recently shown to contain significant alterations in the intracellular distribution of actin (R. Pollack and L. Kopelovich, in preparation), and elevated levels of plasminogen activator (L. Kopelovich).
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PMID:Recent studies on the identification of proliferative abnormalities and of oncogenic potential of cutaneous cells in individuals at increased risk of colon cancer. 1 61

Treatment of the cells of the 311 cell line, a pluripotent mouse teratocarcinoma cell line, with 12-O-tetradecanoylphorbol-13-acetate (TPA) modulates c-mos expression. Transient suppression of 6.1 and 4.6 kilobases (kb) transcripts and activation of 1.8 transcript indicate that TPA mediates concurrently positive and negative regulation of c-mos transcription. The results show that the c-mos gene is a TPA-modulated gene. In addition, a TPA-responsive element (GTGACTCA), which exists in the 5'-flanking region of c-mos gene of Balb/c mice [1,2], is suggested to be involved in this response. However, these changes were not accompanied by early marker changes associated with endodermal cell differentiation, i.e., morphological change, induction of plasminogen activator and suppression of glucose transport activity.
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PMID:Changes of c-mos expression in response to 2-O-tetradecanoylphorbol-13-acetate in undifferentiated teratocarcinoma cells. 284 70

The treatment of 311 cells, a pluripotent mouse teratocarcinoma cell line, with a new type of inducer, 3,5-di-tert-butylchalcone 4'-carboxylic acid (Ch55), results in the suppression of the c-mos gene, accompanied by early marker changes associated with cell differentiation, i.e., the enhanced secretion of plasminogen activator and the decrease in peanut agglutinin receptors and glucose transport. This indicates that Ch55 is a potent inducer of teratocarcinoma cells and suppresses c-mos expression.
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PMID:Suppression of c-mos expression in teratocarcinoma cells with a new type of inducer of differentiation, 3,5-di-tert-butylchalcone 4'-carboxylic acid. 296 May 54

The fibrinolytic activity of cancer cells has been repeatedly implicated in mechanisms of local spread and tumour invasiveness. Mononuclear phagocytes associated with solid tumours might also contribute to fibrin dissolution at the tumour/host interface through the expression of plasminogen activator (PA) activity. We have investigated the PA activity of tumour-associated macrophages (TAM) from 4 transplanted murine tumours in syngeneic hosts; peritoneal macrophages (native and thioglycolate-elicited) from both tumour-bearing and control animals were studied as reference cells. TAM from 3 tumours (MSV, mFS6, MN/MCAI) had basal levels of PA activity (20% plasminogen-independent) comparable to or higher than those of thioglycolate-elicited peritoneal macrophages from the same tumour-bearing animals. TAM isolated from 1 tumour (MS2) had a PA which was very low (60% plasminogen-independent), but higher than the activity of unstimulated peritoneal macrophages. Molecular analysis of PA by SDS-PAGE electrophoresis and fibrin autography revealed in all macrophages a single species having an apparent MW of 48 kDA. It thus appears that, in some experimental neoplasms, tumour cell vicinity may represent an in vivo stimulus for macrophage PA expression.
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PMID:Macrophages associated with murine tumours express plasminogen activator activity. 333 72

A panel of human-mouse somatic cell hybrids and specific complementary DNA probes were used to map the human tissue plasminogen activator and urokinase genes to human chromosomes 8 and 10, respectively. This result is in contrast to a previous assignment of a plasminogen activator gene to chromosome 6. As neoplastic cells produce high levels of plasminogen activator, it is of interest that aberrations of chromosome 8 have been linked to various leukemias and lymphomas and that two human oncogenes, c-mos and c-myc, have also been mapped to chromosome 8.
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PMID:Chromosomal locations of human tissue plasminogen activator and urokinase genes. 384 Feb 78

In mouse MSV-3T3 cells the synthesis of the urokinase form of plasminogen activator was increased 10-fold after addition of the tumor promoter phorbol-12-myristate-13-acetate (PMA). PMA also stimulated the secretion of the protein into the culture medium, mostly in the form of enzymatically inactive pro-urokinase. When assayed by injecting RNA into Xenopus laevis oocytes, the concentration of functional urokinase mRNA was found to be 6- to 10-fold higher in the PMA-treated cells; a similar increase in urokinase mRNA content was measured by hybridisation with a mouse urokinase cDNA probe. Thus, the induction of plasminogen activator by PMA in MSV-3T3 cells is accounted for by an increased content of urokinase mRNA.
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PMID:Tumor promoter PMA stimulates the synthesis and secretion of mouse pro-urokinase in MSV-transformed 3T3 cells: this is mediated by an increase in urokinase mRNA content. 654 Nov 26

During oogenesis, mRNA is actively transcribed and accumulated in growing oocytes, but this transcription stops before the oocytes grow to their full size. The accumulated maternal mRNA is used for protein synthesis in the oocytes during meiotic maturation and even in the embryos to sustain development after fertilization. Therefore, the degradation of accumulated maternal mRNA starts during meiotic maturation, but its rate is slow. Nevertheless, some mRNA species should rapidly degrade after fertilization if they encode proteins that play a role in specific events during meiosis and are detrimental for development after fertilization. In this study, to identify the selective degradation of maternal transcripts after fertilization, we sought mRNAs that are degraded in the early hours after fertilization by constructing an oocyte cDNA library after subtracting the cDNA of embryos at the mid one-cell stage. H1oo, c-mos, tPA (tissue type plasminogen activator gene), and Gdf9 were identified as genes whose transcripts undergo rapid degradation after fertilization. RT-PCR analysis showed that none of these transcripts was expressed during pre-implantation development once they were eliminated, suggesting that the mRNA species that are required for oogenesis, but not for early pre-implantation development, are degraded rapidly after fertilization. Microinjection of chimeric mRNAs in which the coding and 3'-untranslated regions (3'UTR) were exchanged between c-mos and hypoxanthine phosphoribosyltransferase mRNAs revealed that the 3'UTR plays a role in the rapid degradation that occurs after fertilization. Cytoplasmic polyadenylation elements (CPEs) was found near a poly(A) signal in the 3'UTR of all the mRNA species identified as rapidly degrading mRNA. The mechanism for the selective degradation is discussed, in relation to its biological significance.
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PMID:Degradation of maternal mRNA in mouse embryos: selective degradation of specific mRNAs after fertilization. 1609 46