Detail
Článek
Článek online
FT
Medvik - BMČ
  • Je něco špatně v tomto záznamu ?

WNT5A: a motility-promoting factor in Hodgkin lymphoma

F. Linke, S. Zaunig, MM. Nietert, F. von Bonin, S. Lutz, C. Dullin, P. Janovská, T. Beissbarth, F. Alves, W. Klapper, V. Bryja, T. Pukrop, L. Trümper, J. Wilting, D. Kube,

. 2017 ; 36 (1) : 13-23. [pub] 20160606

Jazyk angličtina Země Anglie, Velká Británie

Typ dokumentu časopisecké články

Perzistentní odkaz   https://www.medvik.cz/link/bmc17031684

Classical Hodgkin lymphoma (cHL) has a typical clinical manifestation, with dissemination involving functionally neighboring lymph nodes. The factors involved in the spread of lymphoma cells are poorly understood. Here we show that cHL cell lines migrate with higher rates compared with non-Hodgkin lymphoma cell lines. cHL cell migration, invasion and adhesion depend on autocrine WNT signaling as revealed by the inhibition of WNT secretion with the porcupine inhibitors Wnt-C59/IWP-2, but did not affect cell proliferation. While application of recombinant WNT5A or WNT5A overexpression stimulates HL cell migration, neither WNT10A, WNT10B nor WNT16 did so. Time-lapse studies revealed an amoeboid type of cell migration modulated by WNT5A. Reduced migration distances and velocity of cHL cells, as well as altered movement patterns, were observed using porcupine inhibitor or WNT5A antagonist. Knockdown of Frizzled5 and Dishevelled3 disrupted the WNT5A-mediated RHOA activation and cell migration. Overexpression of DVL3-K435M or inhibition of ROCK (Rho-associated protein kinase) by Y-27632/H1152P disrupted cHL cell migration. In addition to these mechanistic insights into the role of WNT5A in vitro, global gene expression data revealed an increased WNT5A expression in primary HL cells in comparison with normal B-cell subsets and other lymphomas. Furthermore, the activity of both porcupine and WNT5A in cHL cells had an impact on lymphoma development in the chick chorionallantoic membrane assay. Massive bleeding of these lymphomas was significantly reduced after inhibition of WNT secretion by Wnt-C59. Therefore, a model is proposed where WNT signaling has an important role in regulating tumor-promoting processes.

Citace poskytuje Crossref.org

000      
00000naa a2200000 a 4500
001      
bmc17031684
003      
CZ-PrNML
005      
20240516120118.0
007      
ta
008      
171025s2017 enk f 000 0|eng||
009      
AR
024    7_
$a 10.1038/onc.2016.183 $2 doi
035    __
$a (PubMed)27270428
040    __
$a ABA008 $b cze $d ABA008 $e AACR2
041    0_
$a eng
044    __
$a enk
100    1_
$a Linke, F $u Clinic of Hematology and Medical Oncology, University Medical Centre of the Georg-August University of Göttingen, Göttingen, Germany.
245    10
$a WNT5A: a motility-promoting factor in Hodgkin lymphoma / $c F. Linke, S. Zaunig, MM. Nietert, F. von Bonin, S. Lutz, C. Dullin, P. Janovská, T. Beissbarth, F. Alves, W. Klapper, V. Bryja, T. Pukrop, L. Trümper, J. Wilting, D. Kube,
520    9_
$a Classical Hodgkin lymphoma (cHL) has a typical clinical manifestation, with dissemination involving functionally neighboring lymph nodes. The factors involved in the spread of lymphoma cells are poorly understood. Here we show that cHL cell lines migrate with higher rates compared with non-Hodgkin lymphoma cell lines. cHL cell migration, invasion and adhesion depend on autocrine WNT signaling as revealed by the inhibition of WNT secretion with the porcupine inhibitors Wnt-C59/IWP-2, but did not affect cell proliferation. While application of recombinant WNT5A or WNT5A overexpression stimulates HL cell migration, neither WNT10A, WNT10B nor WNT16 did so. Time-lapse studies revealed an amoeboid type of cell migration modulated by WNT5A. Reduced migration distances and velocity of cHL cells, as well as altered movement patterns, were observed using porcupine inhibitor or WNT5A antagonist. Knockdown of Frizzled5 and Dishevelled3 disrupted the WNT5A-mediated RHOA activation and cell migration. Overexpression of DVL3-K435M or inhibition of ROCK (Rho-associated protein kinase) by Y-27632/H1152P disrupted cHL cell migration. In addition to these mechanistic insights into the role of WNT5A in vitro, global gene expression data revealed an increased WNT5A expression in primary HL cells in comparison with normal B-cell subsets and other lymphomas. Furthermore, the activity of both porcupine and WNT5A in cHL cells had an impact on lymphoma development in the chick chorionallantoic membrane assay. Massive bleeding of these lymphomas was significantly reduced after inhibition of WNT secretion by Wnt-C59. Therefore, a model is proposed where WNT signaling has an important role in regulating tumor-promoting processes.
650    _2
$a zvířata $7 D000818
650    _2
$a biopsie $7 D001706
650    _2
$a buněčná adheze $x genetika $7 D002448
650    _2
$a nádorové buněčné linie $7 D045744
650    _2
$a pohyb buněk $x genetika $7 D002465
650    _2
$a proliferace buněk $7 D049109
650    _2
$a protein dishevelled $x metabolismus $7 D000072261
650    _2
$a frizzled receptory $x metabolismus $7 D051157
650    _2
$a exprese genu $7 D015870
650    _2
$a Hodgkinova nemoc $x diagnostické zobrazování $x genetika $x metabolismus $x patologie $7 D006689
650    _2
$a lidé $7 D006801
650    _2
$a biologické modely $7 D008954
650    _2
$a dikobrazovití a urzonovití $7 D046328
650    _2
$a signální transdukce $7 D015398
650    _2
$a počítačová rentgenová tomografie $7 D014057
650    _2
$a protein Wnt 5a $x genetika $x metabolismus $7 D000071818
650    _2
$a rhoA protein vázající GTP $x metabolismus $7 D020742
655    _2
$a časopisecké články $7 D016428
700    1_
$a Zaunig, S $u Clinic of Hematology and Medical Oncology, University Medical Centre of the Georg-August University of Göttingen, Göttingen, Germany.
700    1_
$a Nietert, M M $u Department of Medical Statistics, University Medical Centre of the Georg-August University of Göttingen, Göttingen, Germany.
700    1_
$a von Bonin, F $u Clinic of Hematology and Medical Oncology, University Medical Centre of the Georg-August University of Göttingen, Göttingen, Germany.
700    1_
$a Lutz, S $u Institute of Pharmacology, University Medical Centre of the Georg-August University of Göttingen, Göttingen, Germany.
700    1_
$a Dullin, C $u Institute of Diagnostic and Interventional Radiology, University Medical Centre of the Georg-August University of Göttingen, Göttingen, Germany.
700    1_
$a Janovská, P $u Faculty of Science, Institute of Experimental Biology, Masaryk University, Brno, Czech Republic.
700    1_
$a Beissbarth, T $u Department of Medical Statistics, University Medical Centre of the Georg-August University of Göttingen, Göttingen, Germany.
700    1_
$a Alves, F $u Clinic of Hematology and Medical Oncology, University Medical Centre of the Georg-August University of Göttingen, Göttingen, Germany. Institute of Diagnostic and Interventional Radiology, University Medical Centre of the Georg-August University of Göttingen, Göttingen, Germany. Department of Molecular Biology of Neuronal Signals, Max Planck Institute for Experimental Medicine, Göttingen, Germany. $7 gn_A_00005142
700    1_
$a Klapper, Wolfram, $d 1971- $u Section Hematopathology, UKSH Campus Kiel, Kiel, Germany. $7 xx0317360
700    1_
$a Bryja, V $u Faculty of Science, Institute of Experimental Biology, Masaryk University, Brno, Czech Republic. Department of Cytokinetics, Institute of Biophysics, Academy of Sciences of Czech Republic, Brno, Czech Republic.
700    1_
$a Pukrop, T $u Clinic of Hematology and Medical Oncology, University Medical Centre of the Georg-August University of Göttingen, Göttingen, Germany.
700    1_
$a Trümper, Lorenz, $u Clinic of Hematology and Medical Oncology, University Medical Centre of the Georg-August University of Göttingen, Göttingen, Germany. $d 1958- $7 xx0269964
700    1_
$a Wilting, J $u Department of Anatomy and Cell Biology, University Medical Centre of the Georg-August University of Göttingen, Göttingen, Germany.
700    1_
$a Kube, D $u Clinic of Hematology and Medical Oncology, University Medical Centre of the Georg-August University of Göttingen, Göttingen, Germany.
773    0_
$w MED00003600 $t Oncogene $x 1476-5594 $g Roč. 36, č. 1 (2017), s. 13-23
856    41
$u https://pubmed.ncbi.nlm.nih.gov/27270428 $y Pubmed
910    __
$a ABA008 $b sig $c sign $y a $z 0
990    __
$a 20171025 $b ABA008
991    __
$a 20240516120112 $b ABA008
999    __
$a ok $b bmc $g 1255277 $s 992711
BAS    __
$a 3
BAS    __
$a PreBMC
BMC    __
$a 2017 $b 36 $c 1 $d 13-23 $e 20160606 $i 1476-5594 $m Oncogene $n Oncogene $x MED00003600
LZP    __
$a Pubmed-20171025

Najít záznam

Citační ukazatele

Pouze přihlášení uživatelé

Možnosti archivace

Nahrávání dat ...