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Wyszukujesz frazę "WNT" wg kryterium: Temat


Wyświetlanie 1-8 z 8
Tytuł:
Rola komórek macierzystych w etiopatogenezie nowotworów ośrodkowego układu nerwowego
Autorzy:
Rieske, Piotr
Powiązania:
https://bibliotekanauki.pl/articles/1061281.pdf
Data publikacji:
2006
Wydawca:
Medical Communications
Tematy:
APC
P53
SHH
WNT
tumor stem cells
nowotworowe komórki macierzyste
Opis:
The paper presents current views concerning the role of stem cells in neoplasia, with particular emphasis of CNS tumors. First, some arguments are presented supporting the thesis that at the first stage of neoplasia, the cellular target for carcinogens are normal stem cells or progenitor cells. Also, discussed are important problems associated with attempts at identification of cellular sources of neoplasms. One of these is the difficulty encountered with distinguishing stem cells and non-differentiated cells. Second, data are presented allowing the conclusion that within neoplastic tissue exist neoplastic stem cells - cells enabling regeneration of this pathological tissue. In the context of discussion concerning the role of stem cells in the pathogenesis of neoplasms, a new theory about physiologic and pathologic role of normal and damaged proteins, e.g. APC, SUFU, EGFR, c-MYC, P53 is presented. Discussed is also the role of proteins controlling modification of chromatin, e.g. the Polycomb protein. These proteins are extremely important for the differentiation process. The paper presents also own preliminary experience with the role of stem cells in the pathogenesis of CNS tumors. Finally, presented are premises providing hope for application of knowledge concerning neoplastic stem cells in designing novel modalities of oncologic therapies. Development of such therapies may be based on the search for chemotherapeutic agents which would selectively eliminate neoplastic stem cells. It is also possible to use normal but genetically modified stem cells to detect neoplastic stem cells and to eliminate them.
W artykule przedstawiono aktualne poglądy na temat udziału komórek macierzystych w nowotworzeniu, ze szczególnym uwzględnieniem nowotworów ośrodkowego układu nerwowego. Po pierwsze przytoczono niektóre argumenty na rzecz tezy, iż komórkowym celem dla karcynogenów na pierwszym etapie nowotworzenia są prawidłowe komórki macierzyste lub komórki progenitorowe. Jednocześnie omówiono istotne problemy, z jakimi wiążą się próby identyfikacji komórkowego źródła nowotworów. Jednym z nich jest problem odróżnienia komórek macierzystych od komórek zróżnicowanych. Po drugie zaprezentowano dane pozwalające stwierdzić, iż w obrębie tkanki nowotworowej bytują komórki macierzyste nowotworu – komórki umożliwiające regenerację tej patologicznej tkanki. W kontekście rozważań dotyczących roli komórek macierzystych w etiopatogenezie nowotworów przedstawiono nową teorię na temat fizjologicznej i patologicznej roli pełnionej przez prawidłowe i uszkodzone białka, takie jak APC, SUFU, EGFR, c-MYC, P53. Omówione także udział w nowotworzeni, białek kontrolujących modyfikację chromatyny jak np. białka Polycomb. Białka te odgrywają niezwykle istotną rolę w czasie różnicowania. W artykule omówiono także pierwsze doświadczenie własne związane z udziałem komórek macierzystych w etiopatogenezie nowotworów OUN. Wreszcie przedstawione zostały przesłanki dające nadzieję na wykorzystanie wiedzy o nowotworowych komórkach macierzystych do projektowania nowych rodzajów terapii przeciwnowotworowej. Opracowywanie tych terapii może być oparte na poszukiwaniu chemioterapeutyków selektywnie eliminujących nowotworowe komórki macierzyste. Możliwe jest również wykorzystanie prawidłowych, ale zmodyfikowanych genetycznie komórek macierzystych do wyśledzenia nowotworowych komórek macierzystych i ich eliminacji.
Źródło:
Aktualności Neurologiczne; 2006, 6, 3; 169-174
1641-9227
2451-0696
Pojawia się w:
Aktualności Neurologiczne
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
PDZ domain from Dishevelled - a specificity study
Autorzy:
Śmietana, Katarzyna
Mateja, Agnieszka
Krężel, Artur
Otlewski, Jacek
Powiązania:
https://bibliotekanauki.pl/articles/1039926.pdf
Data publikacji:
2011
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
Dishevelled
Cl2FlAsH-EDT2
NES
nuclear export signal
PDZ
Wnt
Opis:
Intracellular signaling cascades induced by Wnt proteins play a key role in developmental processes and are implicated in cancerogenesis. It is still unclear how the cell determines which of the three possible Wnt response mechanisms should be activated, but the decision process is most likely dependent on Dishevelled proteins. Dishevelled family members interact with many diverse targets, however, molecular mechanisms underlying these binding events have not been comprehensively described so far. Here, we investigated the specificity of the PDZ domain from human Dishevelled-2 using C-terminal phage display, which led us to identification of a leucine-rich binding motif strongly resembling the consensus sequence of a nuclear export signal. PDZ interactions with several peptide and protein motifs (including the nuclear export signal sequence from Dishevelled-2 protein) were investigated in detail using fluorescence spectroscopy, mutational analysis and immunoenzymatic assays. The experiments showed that the PDZ domain can bind the nuclear export signal sequence of the Dishevelled-2 protein. Since the intracellular localization of Dishevelled is governed by nuclear localization and nuclear export signal sequences, it is possible that the intramolecular interaction between PDZ domain and the export signal could modulate the balance between nuclear and cytoplasmic pool of the Dishevelled protein. Such a regulatory mechanism would be of utmost importance for the differential activation of Wnt signaling cascades, leading to selective promotion of the nucleus-dependent Wnt β-catenin pathway at the expense of non-canonical Wnt signaling.
Źródło:
Acta Biochimica Polonica; 2011, 58, 2; 243-250
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Expression of RUNX2 and its signaling partners TCF7, FGFR1/2 in cleidocranial dysplasia
Autorzy:
Pawłowska, Elżbieta
Wójcik, Katarzyna
Synowiec, Ewelina
Szczepańska, Joanna
Błasiak, Janusz
Powiązania:
https://bibliotekanauki.pl/articles/1039147.pdf
Data publikacji:
2015
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
RUNX2
Wnt signaling
TCF7
fibroblast growth factor signaling
FGFR1
FGFR2
Opis:
RUNX2 is a member of the PEBP2/CBF transcription factors family controlling the expression of genes whose products are essential for bone formation. Mutations in the RUNX2 gene may be associated with cleidocranial dysplasia (CCD), a rare skeletal disease characterized by stature aberrations, delayed closure of the cranial sutures, hypoplastic or aplastic clavicles, and multiple dental abnormalities. As RUNX2 is involved in many signaling pathways, we hypothesize that CCD may be associated with their changes. We determined the expression of RUNX2 and its signaling partners TCF7, involved in canonical Wnt signaling, and fibroblast growth factor receptors, FGFR1 and FGFR2 in periodontum of CCD patients and control individuals. We did not observe any differences between the level of RUNX2, TCF7 and FGFR1/2 mRNA, determined by real-time PCR, in CDD patients and controls. Therefore, RUNX2 signaling pathways with their partners TCF7 and FGFR1/2 may not be involved in CCD pathogenesis.
Źródło:
Acta Biochimica Polonica; 2015, 62, 1; 123-126
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Magazyn konsygnacyjny w Polsce
Call off stock in Poland
Autorzy:
Gogol, Mateusz
Powiązania:
https://bibliotekanauki.pl/articles/617797.pdf
Data publikacji:
2017
Wydawca:
Uniwersytet Łódzki. Wydawnictwo Uniwersytetu Łódzkiego
Tematy:
magazyn konsygnacyjny
wewnątrzwspólnotowe nabycie towarów (WNT)
call of stock
consignment stock
Opis:
The article presents the conditions for the call of stock in Poland, discusses the rules and problems related to the call of stock , describes the main mistakes made by the legislator and suggests proposed legislative changes that will facilitate the use of call of stock for a larger group of taxpayers.
W artykule przedstawiono warunki funkcjonowania magazynu konsygnacyjnego w Polsce, omówiono przepisy i problemy związane z jego funkcjonowaniem, opisano główne błędy popełnione przez ustawodawcę i wskazano proponowane zmiany legislacyjne, które ułatwią korzystanie z magazynu konsygnacyjnego większej grupie podatników.
Źródło:
Kwartalnik Prawa Podatkowego; 2017, 4; 55-75
1509-877X
Pojawia się w:
Kwartalnik Prawa Podatkowego
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Crosstalk between the TGF-β and WNT signalling pathways during cardiac fibrogenesis
Autorzy:
Działo, Edyta
Tkacz, Karolina
Błyszczuk, Przemysław
Powiązania:
https://bibliotekanauki.pl/articles/1038355.pdf
Data publikacji:
2018
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
TGF-beta
Smad
WNT
beta-catenin
RhoA-ROCK
p38
JNK
Erk1/2
MAPK
cardiac fibrosis
tissue remodelling
cardiac fibroblasts
heart
Opis:
Cardiac fibrosis is referred to as an excessive accumulation of stromal cells and extracellular matrix proteins in the myocardium. Progressive fibrosis causes stiffening of the cardiac tissue and affects conduction of electrical impulses, leading to heart failures in a broad range of cardiac conditions. At the cellular level, activation of the cardiac stromal cells and myofibroblast formation are considered as hallmarks of fibrogenesis. At the molecular level, transforming growth factor β (TGF-β) is traditionally considered as a master regulator of the profibrotic processes. More recently, the WNT signalling pathway has also been found to be implicated in the development of myocardial fibrosis. In this review, we summarize current knowledge on the involvement of TGF-β and WNT downstream molecular pathways to cardiac fibrogenesis and describe a crosstalk between these two profibrotic pathways. TGF-β and WNT ligands bind to different receptors and trigger various outputs. However, a growing body of evidence points to cross-regulation between these two pathways. It has been recognized that in cardiac pathologies TGF-β activates WNT/β-catenin signalling, which in turn stabilizes the TGF-β/Smad response. Furthermore both, the non-canonical TGF-β and non-canonical WNT signalling pathways, activate the same mitogen-activated protein kinases (MAPKs): the extracellular signal-regulated kinase (Erk), the c-Jun N-terminal kinases (JNKs) and p38. The crosstalk between TGF-β and WNT pathways seems to play an essential role in switching on the genetic machinery initiating profibrotic changes in the heart. Better understanding of these mechanisms will open new opportunities for development of targeted therapeutic approaches against cardiac fibrosis in the future.
Źródło:
Acta Biochimica Polonica; 2018, 65, 3; 341-349
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Inhibitory effect of selenomethionine on carcinogenesis in the model of human colorectal cancer in vitro and its link to the Wnt/β-catenin pathway
Autorzy:
Korbut, Edyta
Ptak-Belowska, Agata
Brzozowski, Tomasz
Powiązania:
https://bibliotekanauki.pl/articles/1038360.pdf
Data publikacji:
2018
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
colorectal cancer
GSK-3β
Wnt/β-catenin pathway
selenium
selenomethionine
Opis:
Selenium compounds have been implicated as anticancer agents; however, the mechanism of their inhibitory action against cancer development has not been extensively investigated. A constitutive activation of the Wnt/β-catenin pathway is a central event in colorectal carcinogenesis. In this pathway, excessive cell proliferation is initiated by generation of β-catenin followed by overexpression of proto-oncogenes, such as c-Myc. It is believed that under physiological conditions the level of c-Myc is efficiently controlled by accessibility of the β-catenin protein through the process of phosphorylation by glycogen synthase kinase 3β (GSK-3β). Here, we determined whether selenomethionine (SeMet) can inhibit cell growth and affect the Wnt/β-catenin pathway in the HT-29 human colorectal cancer cells in vitro. The effective cytotoxic doses of SeMet have been selected after 48 h of incubation of this compound with colorectal cancer HT-29 cell line. MTT assay was used to assess cell viability and the protein and mRNA levels of β-catenin and c-Myc were determined by Western blotting and qPCR, respectively. SeMet potently inhibited growth of HT-29 cells, significantly decreased level of the β-catenin protein and mRNA concentration, down-regulated the c-Myc gene expression and up-regulated the pro-apoptotic Bax protein level. Moreover, SeMet increased the level of GSK-3β phosphorylated at serine 9 (S9) and significantly increased the level of β-catenin phosphorylated at S33 and S37. We conclude that SeMet suppresses growth of HT-29 colorectal cancer cells by a mechanism linked to the Wnt/β-catenin pathway, however, degradation of β-catenin may occur independently of GSK-3β catalytic activity and its phosphorylation status.
Źródło:
Acta Biochimica Polonica; 2018, 65, 3; 359-366
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
THE EFFECT OF NICLOSAMIDE ON THE HEAD AND NECK CARCINOMA CELLS SURVIVAL AND THE EXPRESSION OF WNT/β-CATENIN SIGNALING AND GLYCOLYSIS PATHWAY COMPONENTS
Autorzy:
Kleszcz, Robert
Paluszczak, Jarosław
Baer-Dubowska, Wanda
Powiązania:
https://bibliotekanauki.pl/articles/895272.pdf
Data publikacji:
2019-08-30
Wydawca:
Polskie Towarzystwo Farmaceutyczne
Tematy:
Wnt signaling
glycolysis
β-catenin
niclosamide
head and neck carcinoma
Opis:
The aim of this study was to evaluate the effect of niclosamide, an antihelminthic drug recently identified as potential anti-cancer agent, on head and neck squamous carcinoma cells (HNSCC) viability, cell cycle distribution and apoptosis. The expression of key components of Wnt (CTNNB1, GSK-3β, CCND1, c-MYC, MMP7, BIRC5, Axin2) and glycolysis (GLUT1, MCT1, HK2, PFKM, PKM2, PDHA1, PDK1, LDHA) pathways was also examined to assess possible involvement in niclosamide anti-carcinogenic activity. HNSCC cells (FaDu, BICR6, H314 lines) were used in the research. Niclosamide treatment affected hypopharyngeal FaDu cells to the most extent (IC50 = 0.40 µM), while H314 cells derived from the floor of mouth were the least sensitive (IC50 = 0.94 µM). In FaDu cells the increased percentage of the cells in the S phase was observed along with the induction of apoptosis. Treatment with niclosamide in FaDu cells reduced the expression of MMP7 and the majority of glycolytic genes except increased LDHA. These results indicate that niclosamide is efficient inhibitor of HNSCC cells viability, however this effect depends on the cell type. In FaDu cells, the most sensitive to its anti-proliferative effect and prone to cell cycle arrest and apoptosis, this effect might be related to slightly modulation of canonical Wnt signaling and increased expression of LDHA.
Źródło:
Acta Poloniae Pharmaceutica - Drug Research; 2019, 76, 4; 661-669
0001-6837
2353-5288
Pojawia się w:
Acta Poloniae Pharmaceutica - Drug Research
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
THE COMPARISON OF THE EFFECTS OF PANOBINOSTAT AND PKF118-310 ON β-CATENIN-DEPENDENT TRANSCRIPTION IN HEAD AND NECK SQUAMOUS CELL CARCINOMA CELL LINES
Autorzy:
Paluszczak, Jarosław
Kleszcz, Robert
Witczak, Olga
Krajka-Kuźniak, Violetta
Powiązania:
https://bibliotekanauki.pl/articles/895659.pdf
Data publikacji:
2020-02-29
Wydawca:
Polskie Towarzystwo Farmaceutyczne
Tematy:
Wnt signaling
head and neck cancer
panobinostat
PKF118-310
Opis:
Advanced head and neck squamous cell cancers (HNSCC) have unfavorable prognosis and new therapeutic options are necessary to improve treatment outcomes. The Wnt pathway plays an important role in the pathogenesis and progression of HNSCC. The aim of this study was to assess the effects of a histone deacetylase inhibitor – panobinostat on Wnt-dependent gene expression and on cell migration. Cell viability in HNSCC cell lines (BICR6, CAL27, FaDu, H314, SCC-25) was evaluated by MTT assay. The expression of β-catenin-target genes was assessed by qPCR and TCF/LEF-dependent reporter assay. Protein content was evaluated by Western blot. Cell migration was analyzed by the wound healing assay. Panobinostat showed differential modulation of gene expression. It reduced the level of Axin2 in CAL27 and SCC-25 cells but upregulated its expression in BICR6 and H314 cell lines. Moreover, it diminished the expression of MMP7 in BICR6, H314 and CAL27 cell lines. In contrast, the inhibitor of β-catenin transcriptional activity – PKF118-310 down-regulated the expression of β-catenin-target genes in HNSCC cell lines. Interestingly, panobinostat had opposite effects on cell migration in CAL27 and FaDu where it inhibited or stimulated migration, respectively. On the other hand, PKF118-310 reduced cell migration. The anti-cancer effects of panobinostat in HNSCC cells are rather not related to the inhibition of Wnt signaling. PKF118-310 attenuates Wnt signaling, but only in a limited number of HNSCC cell lines. Importantly, the inhibition of Wnt pathway reduces the capacity of cells for migration suggesting that it may potentially therapeutically reduce cell invasion.
Źródło:
Acta Poloniae Pharmaceutica - Drug Research; 2020, 77, 1; 77-88
0001-6837
2353-5288
Pojawia się w:
Acta Poloniae Pharmaceutica - Drug Research
Dostawca treści:
Biblioteka Nauki
Artykuł
    Wyświetlanie 1-8 z 8

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