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[PMID]:29185860
[Au] Autor:Shariatpanahi S; Farahani N; Salehi AR; Salehi R
[Ad] Endereço:a Azad University of Qom , Qom , Isfahan , Iran.
[Ti] Título:High prevalence of mouse mammary tumor virus-like gene sequences in breast cancer samples of Iranian women.
[So] Source:Nucleosides Nucleotides Nucleic Acids;36(10):621-630, 2017 Oct 03.
[Is] ISSN:1532-2335
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mouse mammary tumor virus (MMTV) is considered to be responsible for breast tumor development in mice. In several instances sequences homologous to the genome of this virus have been reported in human breast cancer samples. Here we aimed to evaluate MMTV involvement in human breast cancer development. DNA was extracted from 118 formalin fixed and paraffin embedded malignant (n = 59) and benign (n = 59) breast lesions. Using two sets of outer and inner MMTV-like envelope specific primers, in a nested PCR setup, MMTV genome was detected in 19 samples out of 59 (%32.2) cases of breast carcinomas, while in non-malignant breast tissue samples, only 3 samples out of 59 (%5) were positive. The difference was statistically highly significant (p < 0.001). Alignment of PCR amplified sequences with BR6, GR and C3H mouse mammary tumor virus strains emerged to be around 99% identical which is indicative of tumor tissue infection by an exogenous mouse MMTV genome.
[Mh] Termos MeSH primário: Neoplasias da Mama/genética
Neoplasias da Mama/virologia
Vírus do Tumor Mamário do Camundongo/genética
[Mh] Termos MeSH secundário: Sequência de Bases
Feminino
Seres Humanos
Irã (Geográfico)
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180105
[Lr] Data última revisão:
180105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171130
[St] Status:MEDLINE
[do] DOI:10.1080/15257770.2017.1360498


  2 / 3379 MEDLINE  
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[PMID]:28813660
[Au] Autor:Denzin LK; Khan AA; Virdis F; Wilks J; Kane M; Beilinson HA; Dikiy S; Case LK; Roopenian D; Witkowski M; Chervonsky AV; Golovkina TV
[Ad] Endereço:Child Health Institute of NJ, Department of Pediatrics, Rutgers Robert Wood Johnson Medical School, Rutgers, The State University of NJ, New Brunswick, NJ 08901, USA.
[Ti] Título:Neutralizing Antibody Responses to Viral Infections Are Linked to the Non-classical MHC Class II Gene H2-Ob.
[So] Source:Immunity;47(2):310-322.e7, 2017 Aug 15.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Select humans and animals control persistent viral infections via adaptive immune responses that include production of neutralizing antibodies. The precise genetic basis for the control remains enigmatic. Here, we report positional cloning of the gene responsible for production of retrovirus-neutralizing antibodies in mice of the I/LnJ strain. It encodes the beta subunit of the non-classical major histocompatibility complex class II (MHC-II)-like molecule H2-O, a negative regulator of antigen presentation. The recessive and functionally null I/LnJ H2-Ob allele supported the production of virus-neutralizing antibodies independently of the classical MHC haplotype. Subsequent bioinformatics and functional analyses of the human H2-Ob homolog, HLA-DOB, revealed both loss- and gain-of-function alleles, which could affect the ability of their carriers to control infections with human hepatitis B (HBV) and C (HCV) viruses. Thus, understanding of the previously unappreciated role of H2-O (HLA-DO) in immunity to infections may suggest new approaches in achieving neutralizing immunity to viruses.
[Mh] Termos MeSH primário: Anticorpos Neutralizantes
Antígenos HLA-D/metabolismo
Antígenos de Histocompatibilidade Classe II/metabolismo
Imunidade Humoral
Vírus do Tumor Mamário do Camundongo/imunologia
Vírus Rauscher/imunologia
Infecções por Retroviridae/imunologia
[Mh] Termos MeSH secundário: Animais
Anticorpos Neutralizantes/metabolismo
Anticorpos Antivirais/metabolismo
Apresentação do Antígeno/genética
Biologia Computacional
Feminino
Predisposição Genética para Doença
Antígenos HLA-D/genética
Células HeLa
Hepatite B/imunologia
Hepatite B/transmissão
Hepatite C/imunologia
Hepatite C/transmissão
Antígenos de Histocompatibilidade Classe II/genética
Seres Humanos
Imunidade Humoral/genética
Masculino
Camundongos
Camundongos Endogâmicos
Camundongos Knockout
Mutação/genética
Polimorfismo Genético
Infecções por Retroviridae/transmissão
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Neutralizing); 0 (Antibodies, Viral); 0 (H-2O antigen); 0 (HLA-D Antigens); 0 (HLA-DO antigens); 0 (Histocompatibility Antigens Class II)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170817
[St] Status:MEDLINE


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[PMID]:28809145
[Au] Autor:Konstantoulas CJ; Hagen B; Indik S
[Ad] Endereço:Institute of Virology, University of Veterinary Medicine, Veterinaerplatz 1, 1210 Vienna, Austria.
[Ti] Título:Moderate sensitivity of mouse mammary tumour virus to inhibition by human APOBEC3G.
[So] Source:J Gen Virol;98(9):2362-2367, 2017 Sep.
[Is] ISSN:1465-2099
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Infectivity of the mouse mammary tumour virus (MMTV) is inhibited by mouse APOBEC3 (mA3) which is efficiently packaged into virions. As the inhibition is only partial, the virus can replicate in tissues expressing mA3 and complete its replication cycle. Here, we have examined the sensitivity of MMTV to inhibition by a human orthologue of mA3, A3G. We report that the virus containing A3G is only moderately susceptible to inhibition by the human factor. Whereas the vif-deficient HIV-1 vector produced in human epithelial cells expressing endogenous levels of A3G was efficiently inhibited, an MMTV vector remained fully infectious. Greater A3G expression levels were necessary to restrict infectivity of MMTV, but only when the factor retained its deaminase activity. Furthermore, the spreading kinetic of a replication competent MMTV was only moderately accelerated in cells with downmodulated A3G expression. These data suggest that MMTV has evolved a mechanism to neutralize antiviral activity of APOBEC3 proteins.
[Mh] Termos MeSH primário: Desaminase APOBEC-3G/metabolismo
Vírus do Tumor Mamário do Camundongo/fisiologia
Infecções por Retroviridae/veterinária
Doenças dos Roedores/enzimologia
[Mh] Termos MeSH secundário: Desaminase APOBEC-3G/genética
Animais
Seres Humanos
Vírus do Tumor Mamário do Camundongo/genética
Camundongos
Infecções por Retroviridae/enzimologia
Infecções por Retroviridae/genética
Infecções por Retroviridae/virologia
Doenças dos Roedores/genética
Doenças dos Roedores/virologia
Montagem de Vírus
Replicação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 3.5.4.5 (APOBEC-3G Deaminase); EC 3.5.4.5 (APOBEC3G protein, human); EC 3.5.4.5 (APOBEC3G protein, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170919
[Lr] Data última revisão:
170919
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170816
[St] Status:MEDLINE
[do] DOI:10.1099/jgv.0.000897


  4 / 3379 MEDLINE  
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[PMID]:28351922
[Au] Autor:Byun H; Das P; Yu H; Aleman A; Lozano MM; Matouschek A; Dudley JP
[Ad] Endereço:Department of Molecular Biosciences, The University of Texas at Austin, Austin, Texas, USA.
[Ti] Título:Mouse Mammary Tumor Virus Signal Peptide Uses a Novel p97-Dependent and Derlin-Independent Retrotranslocation Mechanism To Escape Proteasomal Degradation.
[So] Source:MBio;8(2), 2017 Mar 28.
[Is] ISSN:2150-7511
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Multiple pathogens, including viruses and bacteria, manipulate endoplasmic reticulum-associated degradation (ERAD) to avoid the host immune response and promote their replication. The betaretrovirus mouse mammary tumor virus (MMTV) encodes Rem, which is a precursor protein that is cleaved into a 98-amino-acid signal peptide (SP) and a C-terminal protein (Rem-CT). SP uses retrotranslocation for ER membrane extraction and yet avoids ERAD by an unknown mechanism to enter the nucleus and function as a Rev-like protein. To determine how SP escapes ERAD, we used a ubiquitin-activated interaction trap (UBAIT) screen to trap and identify transient protein interactions with SP, including the ERAD-associated p97 ATPase, but not E3 ligases or Derlin proteins linked to retrotranslocation, polyubiquitylation, and proteasomal degradation of extracted proteins. A dominant negative p97 ATPase inhibited both Rem and SP function. Immunoprecipitation experiments indicated that Rem, but not SP, is polyubiquitylated. Using both yeast and mammalian expression systems, linkage of a ubiquitin-like domain (UbL) to SP or Rem induced degradation by the proteasome, whereas SP was stable in the absence of the UbL. ERAD-associated Derlin proteins were not required for SP activity. Together, these results suggested that Rem uses a novel p97-dependent, Derlin-independent retrotranslocation mechanism distinct from other pathogens to avoid SP ubiquitylation and proteasomal degradation. Bacterial and viral infections produce pathogen-specific proteins that interfere with host functions, including the immune response. Mouse mammary tumor virus (MMTV) is a model system for studies of human complex retroviruses, such as HIV-1, as well as cancer induction. We have shown that MMTV encodes a regulatory protein, Rem, which is cleaved into an N-terminal signal peptide (SP) and a C-terminal protein (Rem-CT) within the endoplasmic reticulum (ER) membrane. SP function requires ER membrane extraction by retrotranslocation, which is part of a protein quality control system known as ER-associated degradation (ERAD) that is essential to cellular health. Through poorly understood mechanisms, certain pathogen-derived proteins are retrotranslocated but not degraded. We demonstrate here that MMTV SP retrotranslocation from the ER membrane avoids degradation through a unique process involving interaction with cellular p97 ATPase and failure to acquire cellular proteasome-targeting sequences.
[Mh] Termos MeSH primário: Adenosina Trifosfatases/metabolismo
Evasão da Resposta Imune
Vírus do Tumor Mamário do Camundongo/imunologia
Vírus do Tumor Mamário do Camundongo/fisiologia
Proteínas Nucleares/metabolismo
Complexo de Endopeptidases do Proteassoma/metabolismo
Sinais Direcionadores de Proteínas
Proteínas Virais/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular
Seres Humanos
Proteínas de Membrana/metabolismo
Transporte Proteico
Proteólise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Membrane Proteins); 0 (Nuclear Proteins); 0 (Protein Sorting Signals); 0 (Viral Proteins); 0 (derlin-1 protein, mouse); EC 3.4.25.1 (Proteasome Endopeptidase Complex); EC 3.6.1.- (Adenosine Triphosphatases); EC 3.6.1.- (p97 ATPase)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170330
[St] Status:MEDLINE


  5 / 3379 MEDLINE  
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[PMID]:28253313
[Au] Autor:Szwarc MM; Kommagani R; Peavey MC; Hai L; Lonard DM; Lydon JP
[Ad] Endereço:Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, United States of America.
[Ti] Título:A bioluminescence reporter mouse that monitors expression of constitutively active ß-catenin.
[So] Source:PLoS One;12(3):e0173014, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:This short technical report describes the generation and characterization of a bioluminescence reporter mouse that is engineered to detect and longitudinally monitor the expression of doxycycline-induced constitutively active ß-catenin. The new responder transgenic mouse contains the TetO-ΔN89ß-CatTMILA transgene, which consists of the tet-operator followed by a bicistronic sequence encoding a stabilized form of active ß-catenin (ΔN89ß-catenin), an internal ribosome entry site, and the firefly luciferase gene. To confirm that the transgene operates as designed, TetO-ΔN89ß-CatTMILA transgenic mouse lines were crossed with an effector mouse that harbors the mouse mammary tumor virus-reverse tetracycline transactivator (MMTV-rtTA) transgene (termed MTB hereon), which primarily targets rtTA expression to the mammary epithelium. Following doxycycline administration, the resultant MTB/CatTMILA bigenic reporter exhibited precocious lobuloalveologenesis, ductal hyperplasia, and mammary adenocarcinomas, which were visualized and monitored by in vivo bioluminescence detection. Therefore, we predict that the TetO-ΔN89ß-CatTMILA transgenic responder mouse-when crossed with the appropriate effector transgenic-will have wide-applicability to non-invasively monitor the influence of constitutively active ß-catenin expression on cell-fate specification, proliferation, differentiation, and neoplastic transformation in a broad spectrum of target tissues.
[Mh] Termos MeSH primário: Genes Reporter
beta Catenina/genética
[Mh] Termos MeSH secundário: Animais
Doxiciclina/administração & dosagem
Luminescência
Vírus do Tumor Mamário do Camundongo/genética
Camundongos
Camundongos Transgênicos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (beta Catenin); N12000U13O (Doxycycline)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170912
[Lr] Data última revisão:
170912
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170303
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0173014


  6 / 3379 MEDLINE  
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[PMID]:28194662
[Au] Autor:Christenson JL; Butterfield KT; Spoelstra NS; Norris JD; Josan JS; Pollock JA; McDonnell DP; Katzenellenbogen BS; Katzenellenbogen JA; Richer JK
[Ad] Endereço:Department of Pathology, University of Colorado, Anschutz Medical Campus, 12800 E. 19th Ave., Aurora, CO, 80045, USA.
[Ti] Título:MMTV-PyMT and Derived Met-1 Mouse Mammary Tumor Cells as Models for Studying the Role of the Androgen Receptor in Triple-Negative Breast Cancer Progression.
[So] Source:Horm Cancer;8(2):69-77, 2017 Apr.
[Is] ISSN:1868-8500
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Triple-negative breast cancer (TNBC) has a faster rate of metastasis compared to other breast cancer subtypes, and no effective targeted therapies are currently FDA-approved. Recent data indicate that the androgen receptor (AR) promotes tumor survival and may serve as a potential therapeutic target in TNBC. Studies of AR in disease progression and the systemic effects of anti-androgens have been hindered by the lack of an AR-positive (AR+) immunocompetent preclinical model. In this study, we identified the transgenic MMTV-PyMT (mouse mammary tumor virus-polyoma middle tumor-antigen) mouse mammary gland carcinoma model of breast cancer and Met-1 cells derived from this model as tools to study the role of AR in breast cancer progression. AR protein expression was examined in late-stage primary tumors and lung metastases from MMTV-PyMT mice as well as in Met-1 cells by immunohistochemistry (IHC). Sensitivity of Met-1 cells to the AR agonist dihydrotestosterone (DHT) and anti-androgen therapy was examined using cell viability, migration/invasion, and anchorage-independent growth assays. Late-stage primary tumors and lung metastases from MMTV-PyMT mice and Met-1 cells expressed abundant nuclear AR protein, while negative for estrogen and progesterone receptors. Met-1 sensitivity to DHT and AR antagonists demonstrated a reliance on AR for survival, and AR antagonists inhibited invasion and anchorage-independent growth. These data suggest that the MMTV-PyMT model and Met-1 cells may serve as valuable tools for mechanistic studies of the role of AR in disease progression and how anti-androgens affect the tumor microenvironment.
[Mh] Termos MeSH primário: Neoplasias Pulmonares/patologia
Neoplasias Mamárias Experimentais/metabolismo
Receptores Androgênicos/metabolismo
Neoplasias de Mama Triplo Negativas/metabolismo
[Mh] Termos MeSH secundário: Antagonistas de Androgênios/administração & dosagem
Antagonistas de Androgênios/farmacologia
Animais
Linhagem Celular Tumoral
Núcleo Celular/metabolismo
Proliferação Celular/efeitos dos fármacos
Di-Hidrotestosterona/administração & dosagem
Di-Hidrotestosterona/farmacologia
Progressão da Doença
Feminino
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Neoplasias Pulmonares/secundário
Vírus do Tumor Mamário do Camundongo/fisiologia
Camundongos
Camundongos Transgênicos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AR protein, human); 0 (AR protein, mouse); 0 (Androgen Antagonists); 0 (Receptors, Androgen); 08J2K08A3Y (Dihydrotestosterone)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171025
[Lr] Data última revisão:
171025
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170215
[St] Status:MEDLINE
[do] DOI:10.1007/s12672-017-0285-6


  7 / 3379 MEDLINE  
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[PMID]:28100467
[Au] Autor:Mohapatra B; Zutshi N; An W; Goetz B; Arya P; Bielecki TA; Mustaq I; Storck MD; Meza JL; Band V; Band H
[Ad] Endereço:Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, NE 68198, USA.
[Ti] Título:An essential role of CBL and CBL-B ubiquitin ligases in mammary stem cell maintenance.
[So] Source:Development;144(6):1072-1086, 2017 03 15.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The ubiquitin ligases CBL and CBL-B are negative regulators of tyrosine kinase signaling with established roles in the immune system. However, their physiological roles in epithelial tissues are unknown. Here, we used MMTV-Cre-mediated gene deletion on a null background, as well as a tamoxifen-inducible mammary stem cell (MaSC)-specific and double knockout ( DKO) using Lgr5-EGFP-IRES-CreERT2, to demonstrate a mammary epithelial cell-autonomous requirement of CBL and CBL-B in the maintenance of MaSCs. Using a newly engineered tamoxifen-inducible and deletion model with a dual fluorescent reporter ( ), we show that DKO in mammary organoids leads to hyperactivation of AKT-mTOR signaling with depletion of MaSCs. Chemical inhibition of AKT or mTOR rescued MaSCs from DKO-induced depletion. Our studies reveal a novel, cell-autonomous requirement of CBL and CBL-B in epithelial stem cell maintenance during organ development and remodeling through modulation of mTOR signaling.
[Mh] Termos MeSH primário: Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Glândulas Mamárias Animais/citologia
Proteínas Proto-Oncogênicas c-cbl/metabolismo
Células-Tronco/citologia
[Mh] Termos MeSH secundário: Animais
Autorrenovação Celular/efeitos dos fármacos
Separação Celular
Células Epiteliais/citologia
Células Epiteliais/metabolismo
Feminino
Deleção de Genes
Integrases/metabolismo
Glândulas Mamárias Animais/crescimento & desenvolvimento
Vírus do Tumor Mamário do Camundongo/metabolismo
Camundongos
Camundongos Knockout
Organoides/citologia
Proteínas Proto-Oncogênicas c-akt/metabolismo
Receptores Acoplados a Proteínas-G/metabolismo
Transdução de Sinais
Células-Tronco/metabolismo
Serina-Treonina Quinases TOR/metabolismo
Tamoxifeno/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (Lgr5 protein, mouse); 0 (Receptors, G-Protein-Coupled); 094ZI81Y45 (Tamoxifen); EC 2.3.2.27 (Proto-Oncogene Proteins c-cbl); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 2.7.7.- (Cre recombinase); EC 2.7.7.- (Integrases); EC 6.3.2.19 (Cblb protein, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171126
[Lr] Data última revisão:
171126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170120
[St] Status:MEDLINE
[do] DOI:10.1242/dev.138164


  8 / 3379 MEDLINE  
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[PMID]:28040797
[Au] Autor:Samanta SK; Sehrawat A; Kim SH; Hahm ER; Shuai Y; Roy R; Pore SK; Singh KB; Christner SM; Beumer JH; Davidson NE; Singh SV
[Ad] Endereço:Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
[Ti] Título:Disease Subtype-Independent Biomarkers of Breast Cancer Chemoprevention by the Ayurvedic Medicine Phytochemical Withaferin A.
[So] Source:J Natl Cancer Inst;109(6), 2017 06.
[Is] ISSN:1460-2105
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Background: A nontoxic chemopreventive intervention efficacious against different subtypes of breast cancer is still a clinically unmet need. The present study was undertaken to determine the efficacy of an Ayurvedic medicine phytochemical (Withaferin A, [WA]) for chemoprevention of breast cancer and to elucidate its mode of action. Methods: Chemopreventive efficacy of WA (4 and 8 mg/kg body weight) was determined using a rat model of breast cancer induced by N-methyl-N-nitrosourea (MNU; n = 14 for control group, n = 15 for 4 mg/kg group, and n = 18 for 8 mg/kg group). The mechanisms underlying breast cancer chemoprevention by WA were elucidated by immunoblotting, biochemical assays, immunohistochemistry, and cytokine profiling using plasma and tumors from the MNU-rat (n = 8-12 for control group, n = 7-11 for 4 mg/kg group, and n = 8-12 for 8 mg/kg group) and/or mouse mammary tumor virus-neu (MMTV-neu) models (n = 4-11 for control group and n = 4-21 for 4 mg/kg group). Inhibitory effect of WA on exit from mitosis and leptin-induced oncogenic signaling was determined using MCF-7 and/or MDA-MB-231 cells. All statistical tests were two-sided. Results: Incidence, multiplicity, and burden of breast cancer in rats were decreased by WA administration. For example, the tumor weight in the 8 mg/kg group was lower by about 68% compared with controls (8 mg/kg vs control, mean = 2.76 vs 8.59, difference = -5.83, 95% confidence interval of difference = -9.89 to -1.76, P = .004). Mitotic arrest and apoptosis induction were some common determinants of breast cancer chemoprevention by WA in the MNU-rat and MMTV-neu models. Cytokine profiling showed suppression of plasma leptin levels by WA in rats. WA inhibited leptin-induced oncogenic signaling in cultured breast cancer cells. Conclusions: WA is a promising chemopreventative phytochemical with the ability to inhibit at least two different subtypes of breast cancer.
[Mh] Termos MeSH primário: Neoplasias da Mama/prevenção & controle
Neoplasias Mamárias Experimentais/prevenção & controle
Vírus do Tumor Mamário do Camundongo
Infecções por Retroviridae/complicações
Infecções Tumorais por Vírus/complicações
Vitanolídeos/uso terapêutico
[Mh] Termos MeSH secundário: Acetilcoenzima A/sangue
Animais
Apoptose/efeitos dos fármacos
Biomarcadores Tumorais/análise
Neoplasias da Mama/induzido quimicamente
Neoplasias da Mama/química
Neoplasias da Mama/patologia
Ciclo Celular/efeitos dos fármacos
Citocinas/sangue
Desoxiguanosina/análogos & derivados
Desoxiguanosina/análise
Complexo III da Cadeia de Transporte de Elétrons/metabolismo
Feminino
Fatores de Transcrição Forkhead/análise
Seres Humanos
Antígeno Ki-67/análise
Ácido Láctico/sangue
Leptina/sangue
Células MCF-7
Malatos/sangue
Neoplasias Mamárias Experimentais/química
Neoplasias Mamárias Experimentais/patologia
Neoplasias Mamárias Experimentais/virologia
Metilnitrosoureia
Camundongos
Mitose/efeitos dos fármacos
Índice Mitótico
Ratos
Receptores Estrogênicos/análise
Retinal Desidrogenase/análise
Transdução de Sinais/efeitos dos fármacos
Carga Tumoral
Vitanolídeos/análise
Vitanolídeos/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Cytokines); 0 (Forkhead Transcription Factors); 0 (FoxQ1 protein, rat); 0 (Ki-67 Antigen); 0 (Leptin); 0 (Malates); 0 (Receptors, Estrogen); 0 (Withanolides); 33X04XA5AT (Lactic Acid); 684-93-5 (Methylnitrosourea); 72-89-9 (Acetyl Coenzyme A); 817L1N4CKP (malic acid); 88847-89-6 (8-oxo-7-hydrodeoxyguanosine); EC 1.10.2.2 (Electron Transport Complex III); EC 1.2.1.36 (RALDH1 protein, rat); EC 1.2.1.36 (Retinal Dehydrogenase); G9481N71RO (Deoxyguanosine); L6DO3QW4K5 (withaferin A)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170801
[Lr] Data última revisão:
170801
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170102
[St] Status:MEDLINE


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[PMID]:27893716
[Au] Autor:Goreczny GJ; Ouderkirk-Pecone JL; Olson EC; Krendel M; Turner CE
[Ad] Endereço:Department of Cell and Developmental Biology, State University of New York Upstate Medical University, Syracuse, NY, USA.
[Ti] Título:Hic-5 remodeling of the stromal matrix promotes breast tumor progression.
[So] Source:Oncogene;36(19):2693-2703, 2017 May 11.
[Is] ISSN:1476-5594
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The remodeling of the stromal extracellular matrix (ECM) has a crucial, but incompletely understood role during tumor progression and metastasis. Hic-5, a focal adhesion scaffold protein, has previously been implicated in tumor cell invasion, proliferation and metastasis. To investigate the role of Hic-5 in breast tumor progression in vivo, Hic-5 mice were generated and crossed with the Mouse Mammary Tumor Virus-Polyoma Middle T-Antigen mouse. Tumors from the Hic-5 ;PyMT mice exhibited increased latency and reduced growth, with fewer lung metastases, as compared with Hic-5 ;PyMT mice. Immunohistochemical analysis showed that Hic-5 is primarily expressed in the cancer-associated fibroblasts (CAFs). Further analysis revealed that the Hic-5 ;PyMT tumor stroma contains fewer CAFs and exhibits reduced ECM deposition. The remodeling of the stromal matrix by CAFs has been shown to increase tumor rigidity to indirectly regulate FAK Y397 phosphorylation in tumor cells to promote their growth and invasion. Accordingly, the Hic-5 ;PyMT tumor cells exhibited a reduction in FAK Y397 phosphorylation. Isolated Hic-5 ;PyMT CAFs were defective in stress fiber organization and exhibited reduced contractility. These cells also failed to efficiently deposit and organize the ECM in two and three dimensions. This, in turn, impacted three-dimensional MDA-MB-231 tumor cell migration behavior. Thus, using a new knockout mouse model, we have identified Hic-5 expression in CAFs as a key requirement for deposition and remodeling of the stromal ECM to promote non-cell autonomous breast tumor progression.
[Mh] Termos MeSH primário: Neoplasias da Mama/genética
Proteínas do Citoesqueleto/genética
Proteínas de Ligação a DNA/genética
Quinase 1 de Adesão Focal/genética
Proteínas com Domínio LIM/genética
Neoplasias Mamárias Animais/genética
[Mh] Termos MeSH secundário: Animais
Neoplasias da Mama/patologia
Neoplasias da Mama/virologia
Fibroblastos Associados a Câncer/metabolismo
Fibroblastos Associados a Câncer/patologia
Adesão Celular/genética
Proteínas do Citoesqueleto/biossíntese
Proteínas de Ligação a DNA/biossíntese
Progressão da Doença
Matriz Extracelular/genética
Matriz Extracelular/patologia
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Proteínas com Domínio LIM/biossíntese
Neoplasias Mamárias Animais/patologia
Neoplasias Mamárias Animais/virologia
Vírus do Tumor Mamário do Camundongo/genética
Vírus do Tumor Mamário do Camundongo/patogenicidade
Camundongos
Camundongos Knockout
Células Estromais/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytoskeletal Proteins); 0 (DNA-Binding Proteins); 0 (LIM Domain Proteins); 0 (Tgfb1i1 protein, mouse); EC 2.7.10.2 (Focal Adhesion Kinase 1); EC 2.7.10.2 (Ptk2 protein, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161129
[St] Status:MEDLINE
[do] DOI:10.1038/onc.2016.422


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[PMID]:27902734
[Au] Autor:Grosset AA; Poirier F; Gaboury L; St-Pierre Y
[Ad] Endereço:INRS-Institut Armand-Frappier, Laval, QC, Canada.
[Ti] Título:Galectin-7 Expression Potentiates HER-2-Positive Phenotype in Breast Cancer.
[So] Source:PLoS One;11(11):e0166731, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:HER-2 positive tumors are among the most aggressive subtypes of breast cancer and are frequently associated with metastasis and poor outcome. As with other aggressive subtypes of breast cancer, these tumors are associated with abnormally high expression of galectin-7 (gal-7), which confers metastatic breast tumor cells with increased invasive behavior. Although previous studies in the rat model of breast tumorigenesis have shown that gal-7 is also increased in primary breast tumor, its contribution to the development of the primary breast tumors remains unclear. In the present work, we have used genetically-engineered gal-7-deficient mice to examine the role of gal-7 in the development of the mammary gland and of breast cancer. Using histological and immunohistological analysis of whole mammary glands at different stages of development, we detected no significant changes between normal and gal-7-deficient mice. To test the involvement of gal-7 in breast cancer, we next examined the effects of loss of gal-7 on mammary tumor development by crossing gal-7-deficient mice with the mammary tumor transgenic mouse strain FVB-Tg(MMTV-Erbb2)NK1Mul/J. Finally, assessment of mice survival and tumor volume showed a delay of mammary tumor growth in the absence of systemic gal-7. These data suggest that gal-7 could potentiate the phenotype of HER-2 positive primary breast cancer.
[Mh] Termos MeSH primário: Transformação Celular Neoplásica/genética
Galectinas/genética
Glândulas Mamárias Animais/metabolismo
Neoplasias Mamárias Animais/patologia
Receptor ErbB-2/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Proliferação Celular/genética
Modelos Animais de Doenças
Progressão da Doença
Feminino
Seres Humanos
Longevidade/genética
Células MCF-7
Neoplasias Mamárias Animais/mortalidade
Vírus do Tumor Mamário do Camundongo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Galectins); 0 (Lgals7 protein, mouse); EC 2.7.10.1 (Erbb2 protein, mouse); EC 2.7.10.1 (Receptor, ErbB-2)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170705
[Lr] Data última revisão:
170705
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161201
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0166731



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