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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
Content available remote

Involvement of epithelial-mesenchymal transition-inducing transcription factors in the mechanism of Helicobacter pylori-induced fibroblasts activation

100%
Krzysiek-Maczka G., Targosz A., Szczyrk U., Strzalka M., Brzozowski T., Ptak-Belowska A.
Journal of Physiology and Pharmacology
|
2019
|
tom 70
|
nr 5
3

Gamma linolenic acid suppresses hypoxia-induced gastric cancer cell growth and epithelial-mesenchymal transition by inhibiting the Wnt/b-catenin signaling pathway

84%
Wang Y., Shi J., Gong L.
Folia Histochemica et Cytobiologica
|
2020
|
tom 58
|
nr 2
4

ZNF750 inhibits the proliferation and invasion of melanoma cells through modulating the Wnt/beta-catenin signaling pathway

84%
Du Y., LV G., Jing C., Liu J., Liu J.
Folia Histochemica et Cytobiologica
|
2020
|
tom 58
|
nr 4
5

Roles of myeloid-derived suppressor cells in cancer metastasis: immunosuppression and beyond

84%
Khoshbin A. P., Eskian M., Keshavarz-Fathi M., Rezaei N.
Archivum Immunologiae et Therapiae Experimentalis
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2019
|
tom 67
|
nr 2
6

The role of periostin in neoplastic processes

84%
Ratajczak-Wielgomas K., Dziegiel P.
Folia Histochemica et Cytobiologica
|
2015
|
tom 53
|
nr 2
7

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
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tom 56
|
nr 4
8

IL-6 contributes to the TGF-beta1-mediated epithelial to mesenchymal transition in human salivary gland epithelial cells

84%
Sisto M., Tamma R., Ribatti D., Lisi S.
Archivum Immunologiae et Therapiae Experimentalis
|
2020
|
tom 68
|
nr 5
9
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Content available

Recent advances in the role of AMP-activated protein kinase in metabolic reprogramming of metastatic cancer cells: targeting cellular bioenergetics and biosynthetic pathways for anti-tumor treatment

84%
Tyszka-Czochara M., Konieczny P., Majka M.
Journal of Physiology and Pharmacology
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2018
|
tom 69
|
nr 3
10

Znaczenie kliniczne krążących komórek nowotworowych w raku piersi

84%
Kozlowska A., Kozlowski J., Kocki J.
Postępy Biologii Komórki
|
2014
|
tom 41
|
nr 1
11

The Hippo pathway in colorectal cancer

84%
Wierzbicki P. M., Rybarczyk A.
Folia Histochemica et Cytobiologica
|
2015
|
tom 53
|
nr 2
12

Adaptive immune responses associated with breast cancer relapse

84%
Payne K. K., Manjili M. H.
Archivum Immunologiae et Therapiae Experimentalis
|
2012
|
tom 60
|
nr 5
13

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
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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.
14

Leukemia inhibitory factor: a potential biomarker and therapeutic target in pancreatic cancer

84%
Wrona E., Potemski P., Sclafani F., Borowiec M.
Archivum Immunologiae et Therapiae Experimentalis
|
2021
|
tom 69
|
nr 1
15

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
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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.
16
Content available remote

Mechanisms promoting physiological cells progression into tumorigenesis

67%
Korbut E., Ptak-Belowska A., Brzozowski T.
Journal of Physiology and Pharmacology
|
2012
|
tom 63
|
nr 6
17

Differential expression of Snail1 transcription factor and Snail1-related genes in alveolar and embryonal rhabdomyosarcoma subtypes

67%
Puskulluoglu M., Lukasiewicz E., Miekus K., Jarocha D., Majka M.
Folia Histochemica et Cytobiologica
|
2010
|
tom 48
|
nr 4
18

Properties of B16-F10 murine melanoma cells subjected to metabolic stress conditions

67%
Mitrus I., Bryndza E., Kazura M., Smagur A., Sochanik A., Cichon T., Szala S.
Acta Biochimica Polonica
|
2012
|
tom 59
|
nr 3
Neoplastic cells which co-form tumors are usually subjected to various stress factors, mainly hypoxia and shortage of nutrient factors. Such cells employ different strategies that permit their survival under such conditions. Experiments in vitro are usually carried out in the presence of 21% oxygen and medium supplemented with 10% FBS. Altering these parameters can approximate the in vivo conditions found within tumor mass. The present paper reports certain properties (especially ability to metastasize) of B16-F10 cells able to grow upon exposure to altered growth conditions (medium supplemented with 0.06% FBS or presence of 1% oxygen for 24 or 72 hours). These properties were compared with those of control cells cultured in the presence of 21% oxygen and in medium supplemented with 10% FBS. Some properties of the cells exposed to medium supplemented with 0.06% FBS differ from those of cells cultured under low oxygenation conditions (ability to form metastases, to migrate, or to express various proteins). Only the partial deprivation of oxygen did increase both the number of migrating cells and the number of metastases formed. Serum deficiency enhanced only the cell ability to metastasize, but not to migrate. It appears that cultured B16-F10 cells employ different adaptation strategies under conditions of oxygen shortage and those of serum deficiency. Under oxygen deprivation, such cells most likely undergo an epithelial-mesenchymal transition, whereas serum deficiency ("starvation"), while increasing the tumorigenicity of B16-F10 cells, does not induce the epithelial-mesenchymal transition.
19

The anti-tumor activity of E1A and its implications in cancer therapy

67%
Chang Y.-W., Hung M.-C., Su J.-L.
Archivum Immunologiae et Therapiae Experimentalis
|
2014
|
tom 62
|
nr 3
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