Base de dados : MEDLINE
Pesquisa : A11.700 [Categoria DeCS]
Referências encontradas : 244 [refinar]
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[PMID]:29211796
[Au] Autor:Saison-Ridinger M; DelGiorno KE; Zhang T; Kraus A; French R; Jaquish D; Tsui C; Erikson G; Spike BT; Shokhirev MN; Liddle C; Yu RT; Downes M; Evans RM; Saghatelian A; Lowy AM; Wahl GM
[Ad] Endereço:Gene Expression Laboratory, Salk Institute for Biological Studies, La Jolla, California, United States of America.
[Ti] Título:Reprogramming pancreatic stellate cells via p53 activation: A putative target for pancreatic cancer therapy.
[So] Source:PLoS One;12(12):e0189051, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pancreatic ductal adenocarcinoma (PDAC) is characterized by an extremely dense fibrotic stroma, which contributes to tumor growth, metastasis, and drug resistance. During tumorigenesis, quiescent pancreatic stellate cells (PSCs) are activated and become major contributors to fibrosis, by increasing growth factor signaling and extracellular matrix deposition. The p53 tumor suppressor is known to restrict tumor initiation and progression through cell autonomous mechanisms including apoptosis, cell cycle arrest, and senescence. There is growing evidence that stromal p53 also exerts anti-tumor activity by paracrine mechanisms, though a role for stromal p53 in PDAC has not yet been described. Here, we demonstrate that activation of stromal p53 exerts anti-tumor effects in PDAC. We show that primary cancer-associated PSCs (caPSCs) isolated from human PDAC express wild-type p53, which can be activated by the Mdm2 antagonist Nutlin-3a. Our work reveals that p53 acts as a major regulator of PSC activation and as a modulator of PDAC fibrosis. In vitro, p53 activation by Nutlin-3a induces profound transcriptional changes, which reprogram activated PSCs to quiescence. Using immunofluorescence and lipidomics, we have also found that p53 activation induces lipid droplet accumulation in both normal and tumor-associated fibroblasts, revealing a previously undescribed role for p53 in lipid storage. In vivo, treatment of tumor-bearing mice with the clinical form of Nutlin-3a induces stromal p53 activation, reverses caPSCs activation, and decreases fibrosis. All together our work uncovers new functions for stromal p53 in PDAC.
[Mh] Termos MeSH primário: Carcinoma Ductal Pancreático/terapia
Reprogramação Celular
Genes p53
Neoplasias Pancreáticas/terapia
Células Estreladas do Pâncreas/metabolismo
[Mh] Termos MeSH secundário: Animais
Carcinoma Ductal Pancreático/metabolismo
Carcinoma Ductal Pancreático/patologia
Ésteres do Colesterol/metabolismo
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Neoplasias Pancreáticas/metabolismo
Neoplasias Pancreáticas/patologia
Transcrição Genética
Triglicerídeos/metabolismo
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cholesterol Esters); 0 (Triglycerides)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180311
[Lr] Data última revisão:
180311
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171207
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189051


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[PMID]:28461158
[Au] Autor:Yang XP; Liu SL; Xu JF; Cao SG; Li Y; Zhou YB
[Ad] Endereço:Department of Clinical Medicine, Medical College, Qingdao University, Qingdao, Shandong, China.
[Ti] Título:Pancreatic stellate cells increase pancreatic cancer cells invasion through the hepatocyte growth factor /c-Met/survivin regulated by P53/P21.
[So] Source:Exp Cell Res;357(1):79-87, 2017 08 01.
[Is] ISSN:1090-2422
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pancreatic stellate cells (PSCs) are a key cellular component of the pancreatic tumor microenvironment and are considered to contribute to tumor invasion and metastasis. Multiple cytokines and growth factors derived from PSCs are involved in malignant cancer progression, including hepatocyte growth factor (HGF). However, the molecular mechanisms by which HGF regulates cancer invasion and metastasis have not been completely elucidated. Here, we report that two pancreatic cancer (PC) cell lines, Panc-1 and SW1990, displayed different invasive and migratory abilities after treatment with HGF secreted by PSCs. We found that HGF enhanced the invasive and migratory capacity of Panc-1 cells because of P53 deficiency, leading to overexpression of c-Met, which was regulated through P21. Additionally, our data showed that HGF/c-Met-mediated invasion and migration required the upregulation of survivin expression. In conclusion, PSCs promote PC cells invasion and migration via the HGF/c-Met/survivin pathway, which is negatively regulated by P53/P21.
[Mh] Termos MeSH primário: Inibidor de Quinase Dependente de Ciclina p21/metabolismo
Fator de Crescimento de Hepatócito/metabolismo
Proteínas Inibidoras de Apoptose/metabolismo
Células Estreladas do Pâncreas/metabolismo
Proteínas Proto-Oncogênicas c-met/metabolismo
Proteína Supressora de Tumor p53/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Movimento Celular/fisiologia
Seres Humanos
Invasividade Neoplásica
Neoplasias Pancreáticas/metabolismo
Neoplasias Pancreáticas/patologia
Microambiente Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (BIRC5 protein, human); 0 (CDKN1A protein, human); 0 (Cyclin-Dependent Kinase Inhibitor p21); 0 (HGF protein, human); 0 (Inhibitor of Apoptosis Proteins); 0 (TP53 protein, human); 0 (Tumor Suppressor Protein p53); 67256-21-7 (Hepatocyte Growth Factor); EC 2.7.10.1 (MET protein, human); EC 2.7.10.1 (Proto-Oncogene Proteins c-met)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171209
[Lr] Data última revisão:
171209
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE


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[PMID]:29061505
[Au] Autor:Koikawa K; Ohuchida K; Takesue S; Ando Y; Kibe S; Nakayama H; Endo S; Abe T; Okumura T; Horioka K; Sada M; Iwamoto C; Moriyama T; Nakata K; Miyasaka Y; Ohuchida R; Manabe T; Ohtsuka T; Nagai E; Mizumoto K; Hashizume M; Nakamura M
[Ad] Endereço:Department of Surgery and Oncology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
[Ti] Título:Pancreatic stellate cells reorganize matrix components and lead pancreatic cancer invasion via the function of Endo180.
[So] Source:Cancer Lett;412:143-154, 2018 Jan 01.
[Is] ISSN:1872-7980
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Specific cell populations leading the local invasion of cancer are called "leading cells". However, the underlying mechanisms are unclear. Here, we identified leading cells in pancreatic cancer and determined how these cells lead and promote cancer cell invasion in the extracellular matrix (ECM). Using three-dimensional matrix remodeling assay, we found that pancreatic stellate cells (PSCs) frequently invaded the collagen matrix with pancreatic cancer cells (PCCs), which invaded behind the invading PSCs. In addition, invading PSCs changed the alignment of collagen fibers, resulting in ECM remodeling and an increase in the parallel fibers along the direction of invading PSCs. Endo180 expression was higher in PSCs than in PCCs, Endo180 knockdown in PSCs attenuated the invasive abilities of PSCs and co-cultured PCCs, and decreased the expression level of phosphorylated myosin light chain 2 (MLC2). In mouse models, Endo180-knockdown PSCs suppressed tumor growth and changes in collagen fiber orientation in co-transplantation with PCCs. Our findings suggest that PSCs lead the local invasion of PCCs by physically remodeling the ECM, possibly via the function of Endo180, which reconstructs the actin cell skeleton by phosphorylation of MLC2.
[Mh] Termos MeSH primário: Matriz Extracelular/química
Neoplasias Pancreáticas/patologia
Células Estreladas do Pâncreas/fisiologia
Receptores Mitogênicos/fisiologia
[Mh] Termos MeSH secundário: Miosinas Cardíacas/metabolismo
Linhagem Celular Tumoral
Colágeno/química
Seres Humanos
Cadeias Leves de Miosina/metabolismo
Invasividade Neoplásica
Fosforilação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endo180); 0 (Myosin Light Chains); 0 (Receptors, Mitogen); 0 (myosin light chain 2); 9007-34-5 (Collagen); EC 3.6.1.- (Cardiac Myosins)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171205
[Lr] Data última revisão:
171205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171025
[St] Status:MEDLINE


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[PMID]:28827060
[Au] Autor:Ben-Harosh Y; Anosov M; Salem H; Yatchenko Y; Birk R
[Ad] Endereço:Department of Nutrition, Faculty of Health Sciences, Ariel University, Israel.
[Ti] Título:Pancreatic stellate cell activation is regulated by fatty acids and ER stress.
[So] Source:Exp Cell Res;359(1):76-85, 2017 Oct 01.
[Is] ISSN:1090-2422
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Pancreatic pathologies are characterized by a progressive fibrosis process. Pancreatic stellate cells (PSC) play a crucial role in pancreatic fibrogenesis. Endoplasmic reticulum (ER) stress emerges as an important determinant of fibrotic remodeling. Overload of fatty acids (FA), typical to obesity, may lead to lipotoxic state and cellular stress. AIM: To study the effect of different lipolytic challenges on pancreatic ER stress and PSC activation. METHODS: Primary PSCs were exposed to different FAs, palmitate (pal) and oleate (ole), at pathophysiological concentrations typical to obese state, and in acute caerulein-induced stress (cer). PSC activation and differentiation were analyzed by measuring fat accumulation (oil-red staining and quantitation), proliferation (cells count) and migration (wound- healing assay). PSC differentiation markers (α-sma, fibronectin, tgf-ß and collagen secretion), ER stress unfolded protein response and immune indicators (Xbp1, CHOP, TNF-α, IL-6) were analyzed at the transcript and protein expression levels (quantitative RT-PCR and western blotting). RESULTS: PSC exposure to pal and ole FAs (500µM) increased significantly fat accumulation. Proliferation and migration analysis demonstrated that ole FA retained PSC activation, while exposure to pal FA significantly halted proliferation rate and delayed migration. Cer significantly augmented PSC differentiation markers α- sma, fibronectin and collagen, and ER stress and inflammation markers including Xbp1, CHOP, TNF-α and IL-6. The ole FA treatment significantly elevated PSC differentiation markers α-sma, fibronectin and collagen secretion. PSC ER stress was demonstrated following pal treatment with significant elevation of Xbp1 splicing and CHOP levels. CONCLUSION: Exposure to pal FA halted PSC activation and differentiation and elevated ER stress markers, while cer and ole exposure significantly induced activation, differentiation and fibrosis. Thus, dietary FA composition should be considered and optimized to regulate PSC activation and differentiation in pancreatic pathologies.
[Mh] Termos MeSH primário: Estresse do Retículo Endoplasmático/efeitos dos fármacos
Ácidos Graxos/farmacologia
Células Estreladas do Pâncreas/metabolismo
[Mh] Termos MeSH secundário: Actinas/metabolismo
Animais
Biomarcadores/metabolismo
Diferenciação Celular/efeitos dos fármacos
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Colágeno/metabolismo
Imunofluorescência
Masculino
Células Estreladas do Pâncreas/citologia
Células Estreladas do Pâncreas/efeitos dos fármacos
Processamento de RNA/efeitos dos fármacos
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Ratos Sprague-Dawley
Proteína 1 de Ligação a X-Box/genética
Proteína 1 de Ligação a X-Box/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (Biomarkers); 0 (Fatty Acids); 0 (RNA, Messenger); 0 (X-Box Binding Protein 1); 0 (Xbp1 protein, rat); 0 (smooth muscle actin, rat); 9007-34-5 (Collagen)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170823
[St] Status:MEDLINE


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[PMID]:28605029
[Au] Autor:Melstrom LG; Salazar MD; Diamond DJ
[Ad] Endereço:Department of Surgery and Experimental Therapeutics, City of Hope National Medical Center, Duarte, California.
[Ti] Título:The pancreatic cancer microenvironment: A true double agent.
[So] Source:J Surg Oncol;116(1):7-15, 2017 Jul.
[Is] ISSN:1096-9098
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The tumor microenvironment in pancreatic cancer is a complex balance of pro- and anti-tumor components. The dense desmoplasia consists of immune cells, extracellular matrix, growth factors, cytokines, and cancer associated fibroblasts (CAF) or pancreatic stellate cells (PSC). There are a multitude of targets including hyaluronan, angiogenesis, focal adhesion kinase (FAK), connective tissue growth factor (CTGF), CD40, chemokine (C-X-C motif) receptor 4 (CXCR-4), immunotherapy, and Vitamin D. The developing clinical therapeutics will be reviewed.
[Mh] Termos MeSH primário: Neoplasias Pancreáticas/patologia
Microambiente Tumoral
[Mh] Termos MeSH secundário: Adenocarcinoma/tratamento farmacológico
Adenocarcinoma/patologia
Inibidores da Angiogênese/farmacologia
Bloqueadores do Receptor Tipo 1 de Angiotensina II/farmacologia
Linfócitos T CD4-Positivos/patologia
Linfócitos T CD8-Positivos/patologia
Fibroblastos Associados a Câncer/patologia
Carcinogênese
Transformação Celular Neoplásica
Ensaios Clínicos como Assunto
Fator de Crescimento do Tecido Conjuntivo/antagonistas & inibidores
Proteína-Tirosina Quinases de Adesão Focal/antagonistas & inibidores
Proteínas Hedgehog/antagonistas & inibidores
Seres Humanos
Ácido Hialurônico/metabolismo
Imunoterapia
Macrófagos/patologia
Células Mieloides/patologia
Neutrófilos/patologia
Osteonectina/antagonistas & inibidores
Neoplasias Pancreáticas/tratamento farmacológico
Células Estreladas do Pâncreas/patologia
Vitamina D/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Angiogenesis Inhibitors); 0 (Angiotensin II Type 1 Receptor Blockers); 0 (Hedgehog Proteins); 0 (Osteonectin); 0 (SPARC protein, human); 139568-91-5 (Connective Tissue Growth Factor); 1406-16-2 (Vitamin D); 9004-61-9 (Hyaluronic Acid); EC 2.7.10.2 (Focal Adhesion Protein-Tyrosine Kinases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170613
[St] Status:MEDLINE
[do] DOI:10.1002/jso.24643


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[PMID]:28551708
[Au] Autor:Jagannath S; Garg PK
[Ad] Endereço:Department of Gastroenterology, All India Institute of Medical Sciences, New Delhi, India.
[Ti] Título:Novel and Experimental Therapies in Chronic Pancreatitis.
[So] Source:Dig Dis Sci;62(7):1751-1761, 2017 Jul.
[Is] ISSN:1573-2568
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Chronic pancreatitis (CP) is a progressive inflammatory disease of the pancreas. The currently available treatment of CP is aimed at controlling symptoms and managing complications. Unfortunately, no specific treatment is available to halt the progression of the disease process because the pathophysiological perturbations in CP are not well understood. In this review, we discuss various therapeutic targets and investigational agents acting on these targets. Among these, therapies modulating immune cells and those acting on pancreatic stellate cells appear promising and may translate into clinical benefit in near future. However, these experimental therapies are mostly in animal models and they do not recapitulate all aspects of human disease. Still they may be beneficial in developing effective therapeutic modalities to curb inflammation in chronic pancreatitis.
[Mh] Termos MeSH primário: Imunoterapia/métodos
Pancreatite Crônica/terapia
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Regulação da Expressão Gênica
Seres Humanos
Células Estreladas do Pâncreas
Pancreatite Crônica/imunologia
Pancreatite Crônica/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170529
[St] Status:MEDLINE
[do] DOI:10.1007/s10620-017-4604-0


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[PMID]:28524160
[Au] Autor:Strell C; Norberg KJ; Mezheyeuski A; Schnittert J; Kuninty PR; Moro CF; Paulsson J; Schultz NA; Calatayud D; Löhr JM; Frings O; Verbeke CS; Heuchel RL; Prakash J; Johansen JS; Östman A
[Ad] Endereço:Department of Oncology-Pathology, Cancer Center Karolinska (CCK), Karolinska Institutet, Stockholm 17176, Sweden.
[Ti] Título:Stroma-regulated HMGA2 is an independent prognostic marker in PDAC and AAC.
[So] Source:Br J Cancer;117(1):65-77, 2017 Jun 27.
[Is] ISSN:1532-1827
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The HMGA2 protein has experimentally been linked to EMT and cancer stemness. Recent studies imply that tumour-stroma interactions regulate these features and thereby contribute to tumour aggressiveness. METHODS: We analysed 253 cases of pancreatic ductal adenocarcinoma (PDAC) and 155 cases of ampullary adenocarcinoma (AAC) for HMGA2 expression by IHC. The data were correlated with stroma abundance and supplemented by experimental studies. RESULTS: HMGA2 acts as an independent prognostic marker associated with a significantly shorter overall survival in both tumour types. Overall, HMGA2-positivity was more frequent in patients with PDAC than with AAC. The HMGA2 status in tumour cells significantly correlated with the abundance of PDGFRß-defined stroma cells. In vivo co-injection of Panc-1 cancer cells with pancreatic stellate cells increased tumour growth in a manner associated with increased HMGA2 expression. Furthermore, in vitro treatment of Panc-1 with conditioned media from PDGF-BB-activated stellate cells increased their ability to form tumour spheroids. CONCLUSIONS: This study identifies HMGA2 expression in tumour cells as an independent prognostic marker in PDAC and AAC. Correlative data analysis gives novel tissue-based evidence for a heterotypic cross-talk with stroma cells as a possible mechanism for HMGA2 induction, which is further supported by experimental models.
[Mh] Termos MeSH primário: Adenocarcinoma/metabolismo
Carcinoma Ductal Pancreático/metabolismo
Neoplasias do Ducto Colédoco/metabolismo
Proteína HMGA2/metabolismo
Neoplasias Pancreáticas/metabolismo
[Mh] Termos MeSH secundário: Adenocarcinoma/patologia
Idoso
Ampola Hepatopancreática
Animais
Carcinoma Ductal Pancreático/patologia
Linhagem Celular Tumoral
Neoplasias do Ducto Colédoco/patologia
Feminino
Seres Humanos
Imuno-Histoquímica
Masculino
Camundongos
Camundongos SCID
Meia-Idade
Análise Multivariada
Estadiamento de Neoplasias
Transplante de Neoplasias
Neoplasias Pancreáticas/patologia
Células Estreladas do Pâncreas/metabolismo
Prognóstico
Receptor beta de Fator de Crescimento Derivado de Plaquetas/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Células Estromais/metabolismo
Taxa de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (HMGA2 Protein); EC 2.7.10.1 (Receptor, Platelet-Derived Growth Factor beta)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170828
[Lr] Data última revisão:
170828
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170520
[St] Status:MEDLINE
[do] DOI:10.1038/bjc.2017.140


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[PMID]:28442553
[Au] Autor:Daley D; Mani VR; Mohan N; Akkad N; Pandian GSDB; Savadkar S; Lee KB; Torres-Hernandez A; Aykut B; Diskin B; Wang W; Farooq MS; Mahmud AI; Werba G; Morales EJ; Lall S; Wadowski BJ; Rubin AG; Berman ME; Narayanan R; Hundeyin M; Miller G
[Ad] Endereço:S.A. Localio Laboratory, Department of Surgery, New York University School of Medicine, New York, NY 10016.
[Ti] Título:NLRP3 signaling drives macrophage-induced adaptive immune suppression in pancreatic carcinoma.
[So] Source:J Exp Med;214(6):1711-1724, 2017 Jun 05.
[Is] ISSN:1540-9538
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The tumor microenvironment (TME) in pancreatic ductal adenocarcinoma (PDA) is characterized by immune tolerance, which enables disease to progress unabated by adaptive immunity. However, the drivers of this tolerogenic program are incompletely defined. In this study, we found that NLRP3 promotes expansion of immune-suppressive macrophages in PDA. NLRP3 signaling in macrophages drives the differentiation of CD4 T cells into tumor-promoting T helper type 2 cell (Th2 cell), Th17 cell, and regulatory T cell populations while suppressing Th1 cell polarization and cytotoxic CD8 T cell activation. The suppressive effects of NLRP3 signaling were IL-10 dependent. Pharmacological inhibition or deletion of NLRP3, ASC (apoptosis-associated speck-like protein containing a CARD complex), or caspase-1 protected against PDA and was associated with immunogenic reprogramming of innate and adaptive immunity within the TME. Similarly, transfer of PDA-entrained macrophages or T cells from NLRP3 hosts was protective. These data suggest that targeting NLRP3 holds the promise for the immunotherapy of PDA.
[Mh] Termos MeSH primário: Imunidade Adaptativa
Macrófagos/metabolismo
Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo
Neoplasias Pancreáticas/metabolismo
Neoplasias Pancreáticas/patologia
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Proteínas Reguladoras de Apoptose/deficiência
Proteínas Reguladoras de Apoptose/metabolismo
Proteínas Adaptadoras de Sinalização CARD
Carcinoma Ductal Pancreático/metabolismo
Carcinoma Ductal Pancreático/patologia
Caspase 1/deficiência
Caspase 1/metabolismo
Diferenciação Celular
Proliferação Celular
Reprogramação Celular
Deleção de Genes
Seres Humanos
Imunossupressão
Camundongos Endogâmicos C57BL
Proteína Adaptadora de Sinalização NOD2/metabolismo
Células Estreladas do Pâncreas/metabolismo
Células Estreladas do Pâncreas/patologia
Linfócitos T/imunologia
Microambiente Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apoptosis Regulatory Proteins); 0 (CARD Signaling Adaptor Proteins); 0 (Card15 protein, mouse); 0 (NLR Family, Pyrin Domain-Containing 3 Protein); 0 (NLRP3 protein, human); 0 (Nlrp3 protein, mouse); 0 (Nod2 Signaling Adaptor Protein); 0 (Pycard protein, mouse); EC 3.4.22.36 (Caspase 1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170427
[St] Status:MEDLINE
[do] DOI:10.1084/jem.20161707


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[PMID]:28400334
[Au] Autor:Wang L; Wu H; Wang L; Zhang H; Lu J; Liang Z; Liu T
[Ad] Endereço:Molecular Pathology Research Center, Department of Pathology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China.
[Ti] Título:Asporin promotes pancreatic cancer cell invasion and migration by regulating the epithelial-to-mesenchymal transition (EMT) through both autocrine and paracrine mechanisms.
[So] Source:Cancer Lett;398:24-36, 2017 Jul 10.
[Is] ISSN:1872-7980
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Pancreatic cancer is histopathologically characterized by excessive desmoplasia induced by pancreatic stellate cells (PSCs). Asporin, an extracellular matrix (ECM) protein, is highly expressed in cancer-associated fibroblasts (CAFs). Asporin expression in PSCs and its roles in PSC-pancreatic cancer cell (PCC) interaction remain unclear. The present study firstly showed that Asporin is highly expressed in activated PSCs and is involved in PSC-mediated invasion and migration of PCCs. Exogenous Asporin interacted with the transmembrane receptor CD44 on PCCs to activate NF-κB/p65 and promoted the epithelial-mesenchymal transition (EMT) in PCCs. Furthermore, AKT and ERK pathways participated in Asporin/CD44-induced NF-κB/p65 activation in pancreatic cancer. Asporin had similar effects on PCCs via an autocrine mechanism. Consistent with our in vitro experiments, we showed that Asporin in peritumoral stroma of pancreatic cancer tissues was associated with poor clinical outcome. In conclusion, this is the first study to show that Asporin promotes EMT, invasion, and migration of PCCs by activating CD44-AKT/ERK-NF-κB pathway in paracrine and autocrine manners. Moreover, our results indicate that Asporin may be a prognostic marker and suggest that targeting the tumor microenvironment represents a promising therapeutic strategy in pancreatic cancer.
[Mh] Termos MeSH primário: Comunicação Autócrina
Biomarcadores Tumorais/metabolismo
Proliferação Celular
Transição Epitelial-Mesenquimal
Proteínas da Matriz Extracelular/metabolismo
Neoplasias Pancreáticas/metabolismo
Comunicação Parácrina
[Mh] Termos MeSH secundário: Idoso
Biomarcadores Tumorais/genética
Linhagem Celular Tumoral
Proteínas da Matriz Extracelular/genética
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Feminino
Seres Humanos
Receptores de Hialuronatos/metabolismo
Masculino
Meia-Idade
Invasividade Neoplásica
Neoplasias Pancreáticas/genética
Neoplasias Pancreáticas/patologia
Células Estreladas do Pâncreas/metabolismo
Células Estreladas do Pâncreas/patologia
Fosforilação
Proteínas Proto-Oncogênicas c-akt/metabolismo
Interferência de RNA
Transdução de Sinais
Células Estromais/metabolismo
Células Estromais/patologia
Fator de Transcrição RelA/metabolismo
Transfecção
Microambiente Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ASPN protein, human); 0 (Biomarkers, Tumor); 0 (CD44 protein, human); 0 (Extracellular Matrix Proteins); 0 (Hyaluronan Receptors); 0 (RELA protein, human); 0 (Transcription Factor RelA); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170413
[St] Status:MEDLINE


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[PMID]:28379317
[Au] Autor:Pang TCY; Xu Z; Pothula S; Becker T; Goldstein D; Pirola RC; Wilson JS; Apte MV
[Ad] Endereço:Pancreatic Research Group, South Western Sydney Clinical School,University of New South Wales, and Ingham Institute of Applied Medical Research, Australia and.
[Ti] Título:Circulating pancreatic stellate (stromal) cells in pancreatic cancer-a fertile area for novel research.
[So] Source:Carcinogenesis;38(6):588-591, 2017 Jun 01.
[Is] ISSN:1460-2180
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Pancreatic stellate cells (PSCs) are known to play an important role in facilitating pancreatic cancer progression-both in terms of local tumour growth as well as the establishment of metastases. We have previously demonstrated that PSCs from the primary cancer seed to distant metastatic sites. We therefore hypothesise that PSCs circulate along with pancreatic cancer cells (circulating tumour cells-CTCs) to help create a growth permissive microenvironment at distant metastatic sites. This review aims to explore the concept of circulating PSCs in pancreatic cancer and suggests future directions for research in this area.
[Mh] Termos MeSH primário: Células Neoplásicas Circulantes/patologia
Neoplasias Pancreáticas/patologia
Células Estreladas do Pâncreas/patologia
Microambiente Tumoral
[Mh] Termos MeSH secundário: Animais
Comunicação Celular
Seres Humanos
Metástase Neoplásica
Células Estromais
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170406
[St] Status:MEDLINE
[do] DOI:10.1093/carcin/bgx030



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