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[PMID]:28465529
[Au] Autor:Hasan MK; Yu J; Chen L; Cui B; Widhopf Ii GF; Rassenti L; Shen Z; Briggs SP; Kipps TJ
[Ad] Endereço:Moores Cancer Center, University of California San Diego, La Jolla, CA, USA.
[Ti] Título:Wnt5a induces ROR1 to complex with HS1 to enhance migration of chronic lymphocytic leukemia cells.
[So] Source:Leukemia;31(12):2615-2622, 2017 Dec.
[Is] ISSN:1476-5551
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:ROR1 (receptor tyrosine kinase-like orphan receptor 1) is a conserved, oncoembryonic surface antigen expressed in chronic lymphocytic leukemia (CLL). We found that ROR1 associates with hematopoietic-lineage-cell-specific protein 1 (HS1) in freshly isolated CLL cells or in CLL cells cultured with exogenous Wnt5a. Wnt5a also induced HS1 tyrosine phosphorylation, recruitment of ARHGEF1, activation of RhoA and enhanced chemokine-directed migration; such effects could be inhibited by cirmtuzumab, a humanized anti-ROR1 mAb. We generated truncated forms of ROR1 and found its extracellular cysteine-rich domain or kringle domain was necessary for Wnt5a-induced HS1 phosphorylation. Moreover, the cytoplamic, and more specifically the proline-rich domain (PRD), of ROR1 was required for it to associate with HS1 and allow for F-actin polymerization in response to Wnt5a. Accordingly, we introduced single amino acid substitutions of proline (P) to alanine (A) in the ROR1 PRD at positions 784, 808, 826, 841 or 850 in potential SH3-binding motifs. In contrast to wild-type ROR1, or other ROR1 mutants, ROR1 had impaired capacity to recruit HS1 and ARHGEF1 to ROR1 in response to Wnt5a. Moreover, Wnt5a could not induce cells expressing ROR1 to phosphorylate HS1 or activate ARHGEF1, and was unable to enhance CLL-cell motility. Collectively, these studies indicate HS1 plays an important role in ROR1-dependent Wnt5a-enhanced chemokine-directed leukemia-cell migration.
[Mh] Termos MeSH primário: Proteínas Sanguíneas/metabolismo
Movimento Celular/imunologia
Leucemia Linfocítica Crônica de Células B/imunologia
Leucemia Linfocítica Crônica de Células B/metabolismo
Complexos Multiproteicos/metabolismo
Receptores Órfãos Semelhantes a Receptor Tirosina Quinase/metabolismo
Proteína Wnt-5a/metabolismo
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Proteínas Sanguíneas/química
Quimiocinas/metabolismo
Seres Humanos
Fosforilação
Ligação Proteica
Domínios e Motivos de Interação entre Proteínas
Receptores Órfãos Semelhantes a Receptor Tirosina Quinase/química
Fatores de Troca de Nucleotídeo Guanina Rho/metabolismo
Células Tumorais Cultivadas
Proteína rhoA de Ligação ao GTP/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ARHGEF1 protein, human); 0 (Blood Proteins); 0 (Chemokines); 0 (HCLS1 protein, human); 0 (Multiprotein Complexes); 0 (Rho Guanine Nucleotide Exchange Factors); 0 (WNT5A protein, human); 0 (Wnt-5a Protein); EC 2.7.10.1 (ROR1 protein, human); EC 2.7.10.1 (Receptor Tyrosine Kinase-like Orphan Receptors); EC 3.6.5.2 (rhoA GTP-Binding Protein)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171215
[Lr] Data última revisão:
171215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1038/leu.2017.133


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[PMID]:28465528
[Au] Autor:Yu J; Chen L; Chen Y; Hasan MK; Ghia EM; Zhang L; Wu R; Rassenti LZ; Widhopf GF; Shen Z; Briggs SP; Kipps TJ
[Ad] Endereço:Moores Cancer Center, University of California-San Diego, La Jolla, CA, USA.
[Ti] Título:Wnt5a induces ROR1 to associate with 14-3-3ζ for enhanced chemotaxis and proliferation of chronic lymphocytic leukemia cells.
[So] Source:Leukemia;31(12):2608-2614, 2017 Dec.
[Is] ISSN:1476-5551
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Wnt5a can activate Rho GTPases in chronic lymphocytic leukemia (CLL) cells by inducing the recruitment of ARHGEF2 to ROR1. Mass spectrometry on immune precipitates of Wnt5a-activated ROR1 identified 14-3-3ζ, which was confirmed by co-immunoprecipitation. The capacity of Wnt5a to induce ROR1 to complex with 14-3-3ζ could be blocked in CLL cells by treatment with cirmtuzumab, a humanized mAb targeting ROR1. Silencing 14-3-3ζ via small interfering RNA impaired the capacity of Wnt5a to: (1) induce recruitment of ARHGEF2 to ROR1, (2) enhance in vitro exchange activity of ARHGEF2 and (3) induce activation of RhoA and Rac1 in CLL cells. Furthermore, CRISPR/Cas9 deletion of 14-3-3ζ in ROR1-negative CLL cell-line MEC1, and in MEC1 cells transfected to express ROR1 (MEC1-ROR1), demonstrated that 14-3-3ζ was necessary for the growth/engraftment advantage of MEC1-ROR1 over MEC1 cells. We identified a binding motif (RSPS SAS) in ROR1 for 14-3-3ζ. Site-directed mutagenesis of ROR1 demonstrated that serine-857 was required for the recruitment of 14-3-3ζ and ARHGEF2 to ROR1, and activation of RhoA and Rac1. Collectively, this study reveals that 14-3-3ζ plays a critical role in Wnt5a/ROR1 signaling, leading to enhanced CLL migration and proliferation.
[Mh] Termos MeSH primário: Proteínas 14-3-3/metabolismo
Quimiotaxia/imunologia
Leucemia Linfocítica Crônica de Células B/etiologia
Leucemia Linfocítica Crônica de Células B/metabolismo
Receptores Órfãos Semelhantes a Receptor Tirosina Quinase/metabolismo
Proteína Wnt-5a/metabolismo
[Mh] Termos MeSH secundário: Transferência Adotiva
Motivos de Aminoácidos
Animais
Sítios de Ligação
Proliferação Celular
Células Cultivadas
Modelos Animais de Doenças
Progressão da Doença
Seres Humanos
Leucemia Linfocítica Crônica de Células B/patologia
Camundongos
Camundongos Knockout
Ligação Proteica
Fatores de Troca de Nucleotídeo Guanina Rho/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (14-3-3 Proteins); 0 (ARHGEF2 protein, human); 0 (Rho Guanine Nucleotide Exchange Factors); 0 (WNT5A protein, human); 0 (Wnt-5a Protein); EC 2.7.10.1 (ROR1 protein, human); EC 2.7.10.1 (Receptor Tyrosine Kinase-like Orphan Receptors)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171215
[Lr] Data última revisão:
171215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1038/leu.2017.132


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[PMID]:28681925
[Au] Autor:Hasegawa D; Wada N; Yoshida S; Mitarai H; Arima M; Tomokiyo A; Hamano S; Sugii H; Maeda H
[Ad] Endereço:Department of Endodontology, Kyushu University Hospital, Kyushu University, Fukuoka, Japan.
[Ti] Título:Wnt5a suppresses osteoblastic differentiation of human periodontal ligament stem cell-like cells via Ror2/JNK signaling.
[So] Source:J Cell Physiol;233(2):1752-1762, 2018 Feb.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Wnt5a, a non-canonical Wnt protein, is known to play important roles in several cell functions. However, little is known about the effects of Wnt5a on osteoblastic differentiation of periodontal ligament (PDL) cells. Here, we examined the effects of Wnt5a on osteoblastic differentiation and associated intracellular signaling in human PDL stem/progenitor cells (HPDLSCs). We found that Wnt5a suppressed expression of bone-related genes (ALP, BSP, and Osterix) and alizarin red-positive mineralized nodule formation in HPDLSCs under osteogenic conditions. Immunohistochemical analysis revealed that a Wnt5a-related receptor, receptor tyrosine kinase-like orphan receptor 2 (Ror2), was expressed in rat PDL tissue. Interestingly, knockdown of Ror2 by siRNA inhibited the Wnt5a-induced downregulation of bone-related gene expression in HPDLSCs. Moreover, Western blotting analysis showed that phosphorylation of the intracellular signaling molecule, c-Jun N-terminal kinase (JNK) was upregulated in HPDLSCs cultured in osteoblast induction medium with Wnt5a, but knockdown of Ror2 by siRNA downregulated the phosphorylation of JNK. We also examined the effects of JNK inhibition on Wnt5a-induced suppression of osteoblastic differentiation of HPDLSCs. The JNK inhibitor, SP600125 inhibited the Wnt5a-induced downregulation of bone-related gene expression in HPDLSCs. Additionally, SP600125 inhibited the Wnt5a-induced suppression of the alizarin red-positive reaction in HPDLSCs. These results suggest that Wnt5a suppressed osteoblastic differentiation of HPDLSCs through Ror2/JNK signaling. Non-canonical Wnt signaling, including Wnt5a/Ror2/JNK signaling, may function as a negative regulator of mineralization, preventing the development of non-physiological mineralization in PDL tissue.
[Mh] Termos MeSH primário: Diferenciação Celular
Proteínas Quinases JNK Ativadas por Mitógeno/metabolismo
Células-Tronco Multipotentes/enzimologia
Osteoblastos/enzimologia
Osteogênese
Ligamento Periodontal/enzimologia
Receptores Órfãos Semelhantes a Receptor Tirosina Quinase/metabolismo
Via de Sinalização Wnt
Proteína Wnt-5a/metabolismo
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular/efeitos dos fármacos
Linhagem Celular
Seres Humanos
Proteínas Quinases JNK Ativadas por Mitógeno/antagonistas & inibidores
Masculino
Células-Tronco Multipotentes/efeitos dos fármacos
Osteoblastos/efeitos dos fármacos
Osteogênese/efeitos dos fármacos
Ligamento Periodontal/citologia
Ligamento Periodontal/efeitos dos fármacos
Fosforilação
Inibidores de Proteínas Quinases/farmacologia
Interferência de RNA
Ratos Sprague-Dawley
Receptores Órfãos Semelhantes a Receptor Tirosina Quinase/genética
Transfecção
Via de Sinalização Wnt/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Protein Kinase Inhibitors); 0 (WNT5A protein, human); 0 (Wnt-5a Protein); EC 2.7.10.1 (Receptor Tyrosine Kinase-like Orphan Receptors); EC 2.7.10.1 (Ror2 protein, mouse); EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170707
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.26086


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[PMID]:28818634
[Au] Autor:Peng H; Nerreter T; Chang J; Qi J; Li X; Karunadharma P; Martinez GJ; Fallahi M; Soden J; Freeth J; Beerli RR; Grawunder U; Hudecek M; Rader C
[Ad] Endereço:Department of Immunology and Microbiology, The Scripps Research Institute, Jupiter, FL 33458, USA.
[Ti] Título:Mining Naïve Rabbit Antibody Repertoires by Phage Display for Monoclonal Antibodies of Therapeutic Utility.
[So] Source:J Mol Biol;429(19):2954-2973, 2017 Sep 15.
[Is] ISSN:1089-8638
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Owing to their high affinities and specificities, rabbit monoclonal antibodies (mAbs) have demonstrated value and potential primarily as basic research and diagnostic reagents, but, in some cases, also as therapeutics. To accelerate access to rabbit mAbs bypassing immunization, we generated a large naïve rabbit antibody repertoire represented by a phage display library encompassing >10 billion independent antibodies in chimeric rabbit/human Fab format and validated it by next-generation sequencing. Panels of rabbit mAbs selected from this library against two emerging cancer targets, ROR1 and ROR2, revealed high diversity, affinity, and specificity. Moreover, ROR1- and ROR2-targeting rabbit mAbs demonstrated therapeutic utility as components of chimeric antigen receptor-engineered T cells, further corroborating the value of the naïve rabbit antibody library as a rich and virtually unlimited source of rabbit mAbs.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/isolamento & purificação
Fatores Imunológicos/isolamento & purificação
[Mh] Termos MeSH secundário: Animais
Anticorpos Monoclonais/uso terapêutico
Antígenos de Neoplasias/imunologia
Linhagem Celular Tumoral
Proliferação Celular
Citocinas/secreção
Testes Imunológicos de Citotoxicidade
Seres Humanos
Fragmentos Fab das Imunoglobulinas/genética
Fatores Imunológicos/uso terapêutico
Imunoterapia/métodos
Biblioteca de Peptídeos
Coelhos
Receptores Órfãos Semelhantes a Receptor Tirosina Quinase/imunologia
Proteínas Recombinantes/isolamento & purificação
Proteínas Recombinantes/uso terapêutico
Linfócitos T/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Antigens, Neoplasm); 0 (Cytokines); 0 (Immunoglobulin Fab Fragments); 0 (Immunologic Factors); 0 (Peptide Library); 0 (Recombinant Proteins); EC 2.7.10.1 (ROR1 protein, human); EC 2.7.10.1 (ROR2 protein, human); EC 2.7.10.1 (Receptor Tyrosine Kinase-like Orphan Receptors)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170819
[St] Status:MEDLINE


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[PMID]:28790171
[Au] Autor:Kamizaki K; Doi R; Hayashi M; Saji T; Kanagawa M; Toda T; Fukada SI; Ho HH; Greenberg ME; Endo M; Minami Y
[Ad] Endereço:From the Division of Cell Physiology, Department of Physiology and Cell Biology, and.
[Ti] Título:The Ror1 receptor tyrosine kinase plays a critical role in regulating satellite cell proliferation during regeneration of injured muscle.
[So] Source:J Biol Chem;292(38):15939-15951, 2017 Sep 22.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The Ror family receptor tyrosine kinases, Ror1 and Ror2, play important roles in regulating developmental morphogenesis and tissue- and organogenesis, but their roles in tissue regeneration in adult animals remain largely unknown. In this study, we examined the expression and function of Ror1 and Ror2 during skeletal muscle regeneration. Using an skeletal muscle injury model, we show that expression of Ror1 and Ror2 in skeletal muscles is induced transiently by the inflammatory cytokines, TNF-α and IL-1ß, after injury and that inhibition of TNF-α and IL-1ß by neutralizing antibodies suppresses expression of and in injured muscles. Importantly, expression of , but not , was induced primarily in Pax7-positive satellite cells (SCs) after muscle injury, and administration of neutralizing antibodies decreased the proportion of Pax7-positive proliferative SCs after muscle injury. We also found that stimulation of a mouse myogenic cell line, C2C12 cells, with TNF-α or IL-1ß induced expression of Ror1 via NF-κB activation and that suppressed expression of Ror1 inhibited their proliferative responses in SCs. Intriguingly, SC-specific depletion of decreased the number of Pax7-positive SCs after muscle injury. Collectively, these findings indicate for the first time that Ror1 has a critical role in regulating SC proliferation during skeletal muscle regeneration. We conclude that Ror1 might be a suitable target in the development of diagnostic and therapeutic approaches to manage muscular disorders.
[Mh] Termos MeSH primário: Músculo Esquelético/lesões
Músculo Esquelético/fisiologia
Receptores Órfãos Semelhantes a Receptor Tirosina Quinase/metabolismo
Regeneração
Células Satélites de Músculo Esquelético/citologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Proliferação Celular
Regulação Enzimológica da Expressão Gênica
Interleucina-1beta/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Desenvolvimento Muscular
NF-kappa B/metabolismo
Fator de Transcrição PAX7/metabolismo
Receptores Órfãos Semelhantes a Receptor Tirosina Quinase/genética
Células Satélites de Músculo Esquelético/metabolismo
Transdução de Sinais
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-1beta); 0 (NF-kappa B); 0 (PAX7 Transcription Factor); 0 (Pax7 protein, mouse); 0 (Tumor Necrosis Factor-alpha); EC 2.7.10.1 (Receptor Tyrosine Kinase-like Orphan Receptors); EC 2.7.10.1 (Ror1 protein, mouse); EC 2.7.10.1 (Ror2 protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171009
[Lr] Data última revisão:
171009
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170810
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.785709


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[PMID]:28650466
[Au] Autor:Roarty K; Pfefferle AD; Creighton CJ; Perou CM; Rosen JM
[Ad] Endereço:Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, USA.
[Ti] Título:Ror2-mediated alternative Wnt signaling regulates cell fate and adhesion during mammary tumor progression.
[So] Source:Oncogene;36(43):5958-5968, 2017 Oct 26.
[Is] ISSN:1476-5594
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cellular heterogeneity is a common feature in breast cancer, yet an understanding of the coexistence and regulation of various tumor cell subpopulations remains a significant challenge in cancer biology. In the current study, we approached tumor cell heterogeneity from the perspective of Wnt pathway biology to address how different modes of Wnt signaling shape the behaviors of diverse cell populations within a heterogeneous tumor landscape. Using a syngeneic TP53-null mouse model of breast cancer, we identified distinctions in the topology of canonical Wnt ß-catenin-dependent signaling activity and non-canonical ß-catenin-independent Ror2-mediated Wnt signaling across subtypes and within tumor cell subpopulations in vivo. We further discovered an antagonistic role for Ror2 in regulating canonical Wnt/ß-catenin activity in vivo, where lentiviral shRNA depletion of Ror2 expression augmented canonical Wnt/ß-catenin signaling activity across multiple basal-like models. Depletion of Ror2 expression yielded distinct phenotypic outcomes and divergent alterations in gene expression programs among different tumors, despite all sharing basal-like features. Notably, we uncovered cell state plasticity and adhesion dynamics regulated by Ror2, which influenced Ras Homology Family Member A (RhoA) and Rho-Associated Coiled-Coil Kinase 1 (ROCK1) activity downstream of Dishevelled-2 (Dvl2). Collectively, these studies illustrate the integration and collaboration of Wnt pathways in basal-like breast cancer, where Ror2 provides a spatiotemporal function to regulate the balance of Wnt signaling and cellular heterogeneity during tumor progression.
[Mh] Termos MeSH primário: Neoplasias da Mama/genética
Proteínas Desgrenhadas/genética
Neoplasias Mamárias Animais/genética
Receptores Órfãos Semelhantes a Receptor Tirosina Quinase/genética
Proteínas rho de Ligação ao GTP/genética
Quinases Associadas a rho/genética
[Mh] Termos MeSH secundário: Animais
Neoplasias da Mama/patologia
Adesão Celular/genética
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Neoplasias Mamárias Animais/patologia
Camundongos
Proteína Supressora de Tumor p53/genética
Via de Sinalização Wnt/genética
beta Catenina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dishevelled Proteins); 0 (Dvl2 protein, mouse); 0 (Tumor Suppressor Protein p53); 0 (beta Catenin); EC 2.7.10.1 (Receptor Tyrosine Kinase-like Orphan Receptors); EC 2.7.10.1 (Ror2 protein, mouse); EC 2.7.11.1 (Rock1 protein, mouse); EC 2.7.11.1 (rho-Associated Kinases); EC 3.6.5.2 (RhoA protein, mouse); EC 3.6.5.2 (rho GTP-Binding Proteins)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170627
[St] Status:MEDLINE
[do] DOI:10.1038/onc.2017.206


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[PMID]:28618961
[Au] Autor:Jiang Z; Jiang C; Yu C; Fang J
[Ad] Endereço:1 Yanbian University Medical College, Yanji, China.
[Ti] Título:MicroRNA-208b inhibits human osteosarcoma progression by targeting ROR2.
[So] Source:Tumour Biol;39(6):1010428317705751, 2017 Jun.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:MicroRNAs are widely involved in cancer progression by inhibiting the expression levels of oncogenes or tumor suppressor genes, and dysregulation of microRNAs may contribute to tumorigenesis. Here, we found that overexpressed miR-208b can reduce the proliferation of human osteosarcoma cell lines U-2OS and Saos-2 by arresting cell cycle progression. The in vivo xenograft tumors induced by Saos-2 cells overexpressing miR-208b had smaller size and grew more slowly than those induced by the control cells. The mobility of U-2OS or Saos-2 cells was also downregulated by miR-208b. MiR-208b targeted a site in the 3' untranslated region of receptor tyrosine kinase-like orphan receptor 2. Inhibition of receptor tyrosine kinase-like orphan receptor 2 suppresses osteosarcoma metastasis in vitro. Recovering the expression levels of receptor tyrosine kinase-like orphan receptor 2 in miR-208b-overexpressed U-2OS or Saos-2 cells attenuated the inhibitory effects of miR-208b. In addition, the expression levels of miR-208b are significantly reduced in human osteosarcoma tissue samples compared to normal tissue samples, and miR-208b levels correlated inversely with receptor tyrosine kinase-like orphan receptor 2 levels. On these bases, we identified that miR-208b targets receptor tyrosine kinase-like orphan receptor 2 gene by which miR-208b can regulate the development of osteosarcoma.
[Mh] Termos MeSH primário: Carcinogênese/genética
MicroRNAs/genética
Osteossarcoma/genética
Receptores Órfãos Semelhantes a Receptor Tirosina Quinase/biossíntese
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Proliferação Celular/genética
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Masculino
Osteossarcoma/patologia
Receptores Órfãos Semelhantes a Receptor Tirosina Quinase/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MIRN208 microRNA, human); 0 (MicroRNAs); EC 2.7.10.1 (ROR2 protein, human); EC 2.7.10.1 (Receptor Tyrosine Kinase-like Orphan Receptors)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170622
[Lr] Data última revisão:
170622
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170617
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317705751


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[PMID]:28515212
[Au] Autor:Pandey P; Bhardwaj A; Babu K
[Ad] Endereço:Department of Biological Sciences, Indian Institute of Science Education and Research (IISER), Mohali, Punjab 140306, India.
[Ti] Título:Regulation of WNT Signaling at the Neuromuscular Junction by the Immunoglobulin Superfamily Protein RIG-3 in .
[So] Source:Genetics;206(3):1521-1534, 2017 07.
[Is] ISSN:1943-2631
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Perturbations in synaptic function could affect the normal behavior of an animal, making it important to understand the regulatory mechanisms of synaptic signaling. Previous work has shown that in Caenorhabditis elegans an immunoglobulin superfamily protein, RIG-3, functions in presynaptic neurons to maintain normal acetylcholine receptor levels at the neuromuscular junction (NMJ). In this study, we elucidate the molecular and functional mechanism of RIG-3. We demonstrate by genetic and BiFC (Bi-molecular Fluorescence Complementation) assays that presynaptic RIG-3 functions by directly interacting with the immunoglobulin domain of the nonconventional Wnt receptor, ROR receptor tyrosine kinase (RTK), CAM-1, which functions in postsynaptic body-wall muscles. This interaction in turn inhibits Wnt/LIN-44 signaling through the ROR/CAM-1 receptor, and allows for maintenance of normal acetylcholine receptor, AChR/ACR-16, levels at the neuromuscular synapse. Further, this work reveals that RIG-3 and ROR/CAM-1 function through the ß-catenin/HMP-2 at the NMJ. Taken together, our results demonstrate that RIG-3 functions as an inhibitory molecule of the Wnt/LIN-44 signaling pathway through the RTK, CAM-1.
[Mh] Termos MeSH primário: Proteínas de Caenorhabditis elegans/metabolismo
Moléculas de Adesão Celular/metabolismo
Junção Neuromuscular/metabolismo
Via de Sinalização Wnt
[Mh] Termos MeSH secundário: Animais
Caenorhabditis elegans/genética
Caenorhabditis elegans/metabolismo
Proteínas de Caenorhabditis elegans/genética
Moléculas de Adesão Celular/genética
Proteínas do Citoesqueleto/genética
Proteínas do Citoesqueleto/metabolismo
Glicoproteínas/genética
Glicoproteínas/metabolismo
Ligação Proteica
Receptores Órfãos Semelhantes a Receptor Tirosina Quinase/genética
Receptores Órfãos Semelhantes a Receptor Tirosina Quinase/metabolismo
Receptores Nicotínicos/genética
Receptores Nicotínicos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Caenorhabditis elegans Proteins); 0 (Cell Adhesion Molecules); 0 (Cytoskeletal Proteins); 0 (Glycoproteins); 0 (HMP-2 protein, C elegans); 0 (LIN-44 protein, C elegans); 0 (RIG-3 protein, C elegans); 0 (Receptors, Nicotinic); 0 (acr-16 protein, C elegans); EC 2.7.10.1 (CAM-1 protein, C elegans); EC 2.7.10.1 (Receptor Tyrosine Kinase-like Orphan Receptors)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170519
[St] Status:MEDLINE
[do] DOI:10.1534/genetics.116.195297


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[PMID]:28475014
[Au] Autor:Xu Y; Ma YH; Pang YX; Zhao Z; Lu JJ; Mao HL; Liu PS
[Ad] Endereço:Department of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Jinan, China.
[Ti] Título:Ectopic repression of receptor tyrosine kinase-like orphan receptor 2 inhibits malignant transformation of ovarian cancer cells by reversing epithelial-mesenchymal transition.
[So] Source:Tumour Biol;39(5):1010428317701627, 2017 May.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Receptor tyrosine kinase-like orphan receptor 2 is an enzyme-linked receptor which specifically modulates WNT5A signaling and plays an important role in tumorigenesis, invasion, and metastasis; however, the precise role of receptor tyrosine kinase-like orphan receptor 2 in cancer is controversial. The purpose of this study was to investigate the expression and role of receptor tyrosine kinase-like orphan receptor 2 in ovarian carcinoma and clarify the biological functions and interactions of receptor tyrosine kinase-like orphan receptor 2 with non-canonical Wnt pathways in ovarian cancer. The result of the human ovary tissue microarray revealed that the receptor tyrosine kinase-like orphan receptor 2-positive rate increased in malignant epithelial ovarian cancers and was extremely higher in the metastatic tumor tissues, which was also higher than that in the malignant ovarian tumor tissues. In addition, high expression of receptor tyrosine kinase-like orphan receptor 2 was closely related with ovarian cancer grading. The expression of receptor tyrosine kinase-like orphan receptor 2 protein was higher in SKOV3 and A2780 cells than OVCAR3 and 3AO cells. Knockdown of receptor tyrosine kinase-like orphan receptor 2 inhibited ovarian cancer cell proliferation, migration, invasion, and induced morphologic as well as digestive state alterations in stably transfected SKOV3 cells. Detailed study further revealed that silencing of receptor tyrosine kinase-like orphan receptor 2 reversed the epithelial-mesenchymal transition and inhibited non-canonical Wnt signaling. Our findings suggest that receptor tyrosine kinase-like orphan receptor 2 may be an important regulator of epithelial-mesenchymal transition, primarily regulated the non-canonical Wnt signaling pathway in ovarian cancer cells, and may display a promising therapeutic target for ovarian cancer.
[Mh] Termos MeSH primário: Carcinogênese/genética
Transição Epitelial-Mesenquimal/genética
Neoplasias Ovarianas/genética
Receptores Órfãos Semelhantes a Receptor Tirosina Quinase/biossíntese
[Mh] Termos MeSH secundário: Idoso
Linhagem Celular Tumoral
Movimento Celular/genética
Proliferação Celular/genética
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Meia-Idade
Neoplasias Ovarianas/patologia
Receptores Órfãos Semelhantes a Receptor Tirosina Quinase/antagonistas & inibidores
Proteína Wnt-5a/biossíntese
Proteína Wnt-5a/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (WNT5A protein, human); 0 (Wnt-5a Protein); EC 2.7.10.1 (ROR2 protein, human); EC 2.7.10.1 (Receptor Tyrosine Kinase-like Orphan Receptors)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170613
[Lr] Data última revisão:
170613
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170506
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317701627


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[PMID]:28408486
[Au] Autor:Karvonen H; Niininen W; Murumägi A; Ungureanu D
[Ad] Endereço:BioMediTech, BMT, University of Tampere, Tampere 33014, Finland.
[Ti] Título:Targeting ROR1 identifies new treatment strategies in hematological cancers.
[So] Source:Biochem Soc Trans;45(2):457-464, 2017 Apr 15.
[Is] ISSN:1470-8752
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Receptor tyrosine kinase-like orphan receptor 1 (ROR1) is a member of the ROR receptor family consisting of two closely related type I transmembrane proteins ROR1 and ROR2. Owing to mutations in their canonical motifs required for proper kinase activity, RORs are classified as pseudokinases lacking detectable catalytic activity. ROR1 stands out for its selective and high expression in numerous blood and solid malignancies compared with a minimal expression in healthy adult tissues, suggesting high potential for this molecule as a drug target for cancer therapy. Current understanding attributes a survival role for ROR1 in cancer cells; however, its oncogenic function is cancer-type-specific and involves various signaling pathways. High interest in ROR1-targeted therapies resulted in the development of ROR1 monoclonal antibodies such as cirmtuzumab, currently in a phase I clinical trial for chronic lymphocytic leukemia. Despite these advances in translational studies, the molecular mechanism employed by ROR1 in different cancers is not yet fully understood; therefore, more insights into the oncogenic role of ROR1 signaling are crucial in order to optimize the use of targeted drugs. Recent studies provided evidence that targeting ROR1 simultaneously with inhibition of B-cell receptor (BCR) signaling is more effective in killing ROR1-positive leukemia cells, suggesting a synergistic correlation between co-targeting ROR1 and BCR pathways. Although this synergy has been previously reported for B-cell acute lymphoblastic leukemia, the molecular mechanism appears rather different. These results provide more insights into ROR1-BCR combinatorial treatment strategies in hematological malignancies, which could benefit in tailoring more effective targeted therapies in other ROR1-positive cancers.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia
Neoplasias Hematológicas/tratamento farmacológico
Terapia de Alvo Molecular/métodos
Proteínas Proto-Oncogênicas c-bcr/antagonistas & inibidores
Receptores Órfãos Semelhantes a Receptor Tirosina Quinase/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Ensaios Clínicos como Assunto
Sinergismo Farmacológico
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Neoplasias Hematológicas/genética
Neoplasias Hematológicas/metabolismo
Seres Humanos
Receptores Órfãos Semelhantes a Receptor Tirosina Quinase/genética
Receptores Órfãos Semelhantes a Receptor Tirosina Quinase/metabolismo
Transdução de Sinais
Pesquisa Médica Translacional
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
EC 2.7.10.1 (ROR1 protein, human); EC 2.7.10.1 (Receptor Tyrosine Kinase-like Orphan Receptors); EC 2.7.11.1 (BCR protein, human); EC 2.7.11.1 (Proto-Oncogene Proteins c-bcr)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170502
[Lr] Data última revisão:
170502
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170415
[St] Status:MEDLINE
[do] DOI:10.1042/BST20160272



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