Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038362 (stomatitis)
 8,852 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We examined the sensitivity of four human germ-cell-tumor cell lines exhibiting different stages of differentiation to human interferons (IFNs) in vitro. The cell lines were derived from two embryonal carcinomas (NEC 8 and NEC 14), a choriocarcinoma (IMa), and a yolk-sac tumor (HUOT). Treatment with poly I:C induced IFN production in IMa and HUOT cells, but not in NEC-8 and NEC-14 cells. In the two embryonal-carcinoma cell lines, the addition of IFN-alpha, IFN-beta, and IFN-gamma did not prevent infection by vesicular stomatitis virus and encephalomyocarditis virus. Also, in these two lines, 2-5A synthetase was not induced by the addition of IFN-alpha. In contrast, both IMa and HUOT showed sensitivity to the antiviral action of IFN-alpha and IFN-beta against the two viruses, and 2-5A synthetase was induced by IFN-alpha. IFNs added at doses of up to 1000 IU/ml had no antiproliferative effect on NEC 8, NEC 14, and HUOT, whereas colony formation by IMa cells was greatly suppressed by all three forms of IFN. These results indicate that the production of and sensitivity to IFN are developmentally regulated and are related to the level of differentiation of human germ-cell stem cells.
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PMID:Sensitivity of human germ-cell-tumor cell lines to human interferons. 243 4

The behavior of human teratocarcinoma cells, and especially their stem cells (embryonal carcinoma cells), may provide insights into the properties of human early embryonic cells. We report here that human recombinant gamma-interferon (IFN-gamma) induced the expression of major histocompatibility complex Class I (HLA-A, B, C) antigens and beta 2-microglobulin in the two human embryonal carcinoma cell lines, 2102Ep cl.4D3 and NTERA-2 cl.D1, and in the yolk sac carcinoma cell line, 1411H; human recombinant IFN-alpha and IFN-beta were less effective inducers of these cell surface molecules. No induction was observed in the gestational choriocarcinoma cell line, JAR. Neither IFN-alpha, IFN-beta, nor IFN-gamma caused growth inhibition, expression of major histocompatibility complex Class II (HLA-DR) antigens, resistance to viral (vesicular stomatitis virus) infection, or expression of 2',5'-oligo(A)synthetase in any of the cells. Also, IFN-gamma neither induced differentiation of NTERA-2 cl.D1 cells, which are pluripotent human stem cells, nor influenced their differentiation induced by retinoic acid. However, developmental regulation of responsiveness to IFN was evident, since IFN-gamma induced higher levels of surface expression of HLA-A, B, C and beta 2-microglobulin in the retinoic acid-induced differentiated NTERA-2 cl.D1 cells than in the undifferentiated parental cells. Also, 2',5'-oligo(A)synthetase was inducible in the NTERA-2 cl.D1 differentiated cells by IFN-alpha and -beta, although not by IFN-gamma, and slight resistance to vesicular stomatitis virus infection was evident in aged cultures of differentiated cells exposed to IFN-alpha. The effect of recombinant mouse IFN-gamma on major histocompatibility complex expression by several murine teratocarcinoma cells was also examined: H-2 Class I (H-2Db), but not class II (I-Ab), antigens were induced in the parietal yolk sac carcinoma lines, PYS and F9Ac cl.9; in cultures of PCC3/A/1 containing both embryonal carcinoma (EC) and differentiated cells; and in cultures of the EC cells, PCC4azaR and PCC4AO, without evidence of differentiation. No induction was observed in the murine EC cell lines, F9 or FA (H-2Kk). Our results indicate that human EC cells, like murine EC cells, exhibit only a partial response to the interferons, and that the extent of this response is developmentally regulated.
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PMID:Induction of class I major histocompatibility complex antigens in human teratocarcinoma cells by interferon without induction of differentiation, growth inhibition, or resistance to viral infection. 302 15

Three kinds of human choriocarcinoma cell lines (BeWo, HCCM-5, and NUC-1) were used for examining the antiviral and antiproliferative activities of human interferons (IFNs) in vitro and in vivo. All of the cell lines showed only low sensitivity to the antiviral action of every IFN-alpha, IFN-beta, and IFN-gamma against vesicular stomatitis virus infection. However, 2-5A synthetase was normally induced by IFN-alpha in all of the cell lines. The [3H]thymidine incorporation of both BeWo and HCCM-5 cells was suppressed in dose-dependent manner at 48 hr after treatment with 1 to 1,000 units (U)/ml of IFN-alpha or IFN-beta and the growth of them was also slightly inhibited when treated continuously with 1,000 U/ml for 6 days in vitro. Another cell line NUC-1 was the least sensitive to these IFNs among the three cell lines. IFN-gamma did not show any antiproliferative effect on these cell lines. The intraperitoneal administration of 5000 or 10,000 U of IFN-beta suppressed the growth of xenografts developed in hamster cheek pouches and subcutis of nude mice when its administration was initiated on the first day of cell inoculation. These results indicate that although some heterogeneities exist among the cell lines choriocarcinoma cells are weakly sensitive to the antiproliferative activity of human IFNs.
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PMID:Effects of human interferons on human choriocarcinoma cells in vitro and in vivo. 373 11

Placental trophoblasts are epithelial cells which undergo physiological fusion and generate syncytia. In this study, a placental choriocarcinoma cell line JAR was infected with two enveloped viruses, Parainfluenza type 3 (P3) or vesicular stomatitis virus (VSV). Both viruses possess a fusion glycoprotein known to be able to induce polykaryon formation in nonpolarized cells. The P3 virus fusion protein was localized on the apical as well as on the basal plasma membrane domains of the infected JAR cells. Infection of the JAR cell monolayer with P3 virus, whose fusion protein is active at pH 7.0, resulted in syncytia formation. Furthermore, the actin ring structure surrounding individual cells disappeared during the P3 virus induced cell-cell fusion. On the contrary, the VSV glycoprotein was found preferentially on the apical plasma membrane domain. To activate the VSV fusogen, the cells were subjected to pH 5.0. However, no syncytia formation peculiar to VSV-infected fibroblasts was observed, and the actin ring structures remained intact. We conclude that in JAR cells the VSV fusion protein exhibits a polarized expression while the P3 virus fusion glycoprotein is distributed between the two membrane domains. Our results suggest that an apically situated fusogen is not sufficient to mediate cell-cell fusion of JAR cells.
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PMID:Polarity and fusion of JAR choriocarcinoma cells as assessed by enveloped viral glycoproteins. 838 1