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1

Epithelial–mesenchymal transition in chronic rhinosinusitis: differences revealed between epithelial cells from nasal polyps and inferior turbinates

100%
Konnecke M., Burmeister M., Pries R., Boscke R., Bruchhage K.-L., Ungefroren H., Klimek L., Wollenberg B.
Archivum Immunologiae et Therapiae Experimentalis
|
2017
|
tom 65
|
nr 2
2

Inhibin-alpha, E-cadherin, calretinin and Ki-67 antigen in the immunohistochemical evaluation of canine and human testicular neoplasms

84%
Ciaputa R., Nowak M., Madej J. A., Poradowski D., Janus I., Dziegiel P., Gorzynska E., Kandefer-Gola M.
Folia Histochemica et Cytobiologica
|
2014
|
tom 52
|
nr 4
3

Biomarkers of epithelial-mesenchymal transition in localized, surgically treated clear-cell renal cell carcinoma

84%
Gasinska A., Jaszczynski J., Adamczyk A., Janecka-Widla A., Wilk W., Cichocka A., Stelmach A.
Folia Histochemica et Cytobiologica
|
2018
|
tom 56
|
nr 4
4

Urothelial cancer of the prostate gland. Immunohistochemical analysis of two cases of rare canine cancer

84%
Ciaputa R., Grieco V., Janus I., Kandefer-Gola M., Dziegiel P., Nowak M.
Folia Histochemica et Cytobiologica
|
2020
|
tom 58
|
nr 4
5

MiR-30b is involved in methylglyoxal-induced epithelial-mesenchymal transition of peritoneal mesothelial cells in rats

84%
Liu H., Zhang N., Tian D.
Cellular and Molecular Biology Letters
|
2014
|
tom 19
|
nr 2
Epithelial-mesenchymal transition (EMT) of peritoneal mesothelial cells (PMC) is a major contributor to the pathogenesis of peritoneal fibrosis. EMT is at least in part caused by repeated exposure to glucose degradation products (GDPs), such as methylglyoxal (MGO). MiRNA contributes greatly to the EMT of PMCs. In this study, we tried to profile whether differences exist between the peritoneal membrane (PM) miRNA expression seen in control rats and that seen in rats injected intraperitoneally with MGO. We assessed whether miR-30b has a possible role in MGO-induced EMT of PMCs in rats. Comparative miRNA expression array and real-time PCR analyses were conducted for the control group at the start of the experiment and for the MGO group after 1 and 2 weeks. During the second week, the MGO rats were treated with: a chemically modified antisense RNA oligonucleotide (ASO) complementary to the mature miR-30b (ASO group); an miR-30b mismatch control sequence (MIS group); or a citrate buffer (EMT group). Bioinformatic analyses indicated that the 3′ untranslated region (3′-UTR) of bone morphogenetic protein 7 (BMP7) mRNA did contain a putative binding site for miR-30b. We also tried to investigate whether miR-30b targeted BMP7 in vitro by transfection. Of the upregulated miRNAs, miR-30b expression demonstrated the greatest increase. The administration of miR-30b ASO for two weeks significantly reduced α-SMA excretion and upregulated E-cadherin and BMP-7 expression. Our in vitro study showed that miR-30b directly targeted and inhibited BMP7 by binding to its 3’-UTR. Our results revealed that miR-30b is involved in MGO-induced EMT of PMCs in rats.
6

Expression of E-cadherin, beta-catenin and Ki-67 antigen and their reciprocal relationships in mammary adenocarcinomas in bitches

84%
Nowak M., Madej J. A., Dziegiel P.
Folia Histochemica et Cytobiologica
|
2007
|
tom 45
|
nr 3
7

High level expression of STAG1-PMEPA1 in an androgen-independent prostate cancer PC3 subclone

84%
Hirokawa Y. S., Takagi A., Uchida K., Kozuka Y., Yoneda M., Watanabe M., Shiraishi T.
Cellular and Molecular Biology Letters
|
2007
|
tom 12
|
nr 3
In this paper, we describe the isolation and characterization of two PC3 subclones. One subclone, mr, showed an epithelial phenotype, the other, M1, showed a sarcomatous morphology. Transplanted into nude mice, mr developed tumors at a dramatically faster rate than M1. Comparing the two subclones, differentially expressed genes were identified, including E-cadherin, IL-8 and STAG1/PMEPA1. These genes were expressed at higher levels in mr than in M1.
8

The effect of TGF-beta1 and Smad7 gene transfer on the phenotypic changes of rat alveolar epithelial cells

84%
Xu G. P., Li Q. Q., Cao X. X., Chen Q., Zhao Z. H., Diao Z. Q., Xu Z. D.
Cellular and Molecular Biology Letters
|
2007
|
tom 12
|
nr 3
The aim of this study was to investigate whether transforming growth factor-β1 (TGF-β1) could induce alveolar epithelial-mesenchymal transition (EMT) in vitro, and whether Smad7 gene transfer could block this transition. We also aimed to elucidate the possible mechanisms of these processes. The Smad7 gene was transfected to the rat type II alveolar epithelial cell line (RLE-6TN). Expression of the EMT-associated markers was assayed by Western Blot and Real-time PCR. Morphological alterations were examined via phase-contrast microscope and fluorescence microscope, while ultrastructural changes were examined via electron microscope. TGF-β1 treatment induced a fibrotic phenotype of RLE-6TN with increased expression of fibronectin (FN), α-smooth muscle actin (α-SMA) and vimentin, and decreased expression of E-cadherin (E-cad) and cytokeratin19 (CK19). After transfecting the RLE-6TN with the Smad7 gene, the expression of the mesenchymal markers was downregulated while that of the epithelial markers was upregulated. TGF-β1 treatment for 48 h resulted in the separation of RLE-6TN from one another and a change into elongated, myofibroblast-like cells. After the RLE-6TN had been transfected with the Smad7 gene, TGF-β1 treatment had no effect on the morphology of the RLE-6TN. TGF-β1 treatment for 48 h resulted in an abundant expression of α-SMA in the RLE-6TN. If the RLE-6TN were transfected with the Smad7 gene, TGF-β1 treatment for 48 h could only induce a low level of α-SMA expression. Furthermore, TGF-β1 treatment for 12 h resulted in the degeneration and swelling of the osmiophilic multilamellar bodies, which were the markers of type II alveolar epithelial cells. TGF-β1 can induce alveolar epithelialmesenchymal transition in vitro, which is dependent on the Smads signaling pathway to a certain extent. Overexpression of the Smad7 gene can partially block this process.
9

Expression of p130cas, E-cadherin and beta-catenin and their correlation with clinicopathological parameters in non-small cell lung cancer: p130cas over-expression predicts poor prognosis

67%
Miao Y., Li A.-L., Wang L., Fan C.-F., Zhang X.-P., Xu H.-T., Han Y., Liu Y., Wang E.-H.
Folia Histochemica et Cytobiologica
|
2012
|
tom 50
|
nr 3
10

E-cadherin immunohistochemical expression in mammary gland neoplasms in bitches

67%
Rodo A., Malicka E.
Polish Journal of Veterinary Sciences
|
2008
|
tom 11
|
nr 1
47-54
The aim of the study was to investigate E-cadherin expression in correlation with other neoplasm traits such as: histological type, the differentiation grade and proliferative activity. Material for the investigation comprised mammary gland tumours, collected from dogs, the patients of veterinary clinics, during surgical procedures and archival samples. All together 21 adenomas, 32 complex carcinomas, 35 simple carcinomas and 13 solid carcinomas were qualified for further investigation. E-cadherin expression was higher in adenomas as compared with carcinomas but lower in solid carcinomas as compared with simple and complex carcinomas. More over, the expression of E-cadherin decreased with the increase in the neoplasm malignancy and proliferative activity (value of the mitotic index and number of cells showing Ki67). The study has shown that the expression of E-cadherin can be used as a prognostic factor.
11
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Cell junction disruption after 36 h milk accumulation was associated with changes in mammary secretory tissue activity and dynamics in lactating dairy goats

67%
Ben C. H., Lacasse P., Marnet P.-G., Wiatr-Letort S., Finot L., Boutinaud M.
Journal of Physiology and Pharmacology. Supplement
|
2009
|
tom 60
|
nr 3
105-111
12

Antileukemic activity of combined epigenetic agents, DNMT inhibitors zebularine and RG108 with HDAC inhibitors, against promyelocytic leukemia HL-60 cells

67%
Savickiene J., Treigyte G., Borutinskaite V.-V., Navakauskiene R.
Cellular and Molecular Biology Letters
|
2012
|
tom 17
|
nr 4
DNMT inhibitors are promising new drugs for cancer therapies. In this study, we have observed the antileukemic action of two diverse DNMT inhibitors, the nucleoside agent zebularine and the non-nucleoside agent RG108, in human promyelocytic leukemia (PML) HL-60 cells. Zebularine but not RG108 caused dose- and time-dependent cell growth inhibition and induction of apoptosis. However, co-treatment with either drug at a non-toxic dose and all trans retinoic acid (RA) reinforced differentiation to granulocytes, while 24 or 48 h-pretreatment with zebularine or RG108 followed by RA alone or in the presence of HDAC inhibitors (sodium phenyl butyrate or BML-210) significantly accelerated and enhanced cell maturation to granulocytes. This occurs in parallel with the expression of a surface biomarker, CD11b, and early changes in histone H4 acetylation and histone H3K4me3 methylation. The application of both drugs to HL-60 cells in continuous or sequential fashion decreased DNMT1 expression, and induced E-cadherin promoter demethylation and reactivation at both the mRNA and the protein levels in association with the induction of granulocytic differentiation. The results confirmed the utility of zebularine and RG108 in combinations with RA and HDAC inhibitors to reinforce differentiation effects in promyelocytic leukemia.
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