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[PMID]:28637122
[Au] Autor:Wang ZG; Mi J; Wang XR; Huo YY; Peng YJ; Zhang HM; Gao Y; Zhang HL
[Ad] Endereço:a Department of Pharmaceutical Analysis , Heilongjiang University of Chinese Medicine , Harbin , China.
[Ti] Título:A new cinnamic acid glycoside from roots of Heracleum dissectum.
[So] Source:Nat Prod Res;32(2):133-140, 2018 Jan.
[Is] ISSN:1478-6427
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:From the roots of Heracleum dissectum Lebb., one new cinnamic acid glycoside derivative named dissectumoside (1), together with eight known compounds including three phenolics, three phenolic glycosides and two phenylpropanoic glycoside were isolated using various chromatographic methods. Among them compound 2-9 was isolated from the plant for the first time. Their structures were elucidated and identified on the basis of their physicochemical properties and by extensive analyses of NMR spectroscopy and high-resolution mass spectrometry. The results of triglyceride accumulation screening in 3T3-L1 cells showed that compounds 1, 5 and 9 exhibited significantly accelerating activities of adipogenesis in adipocytes.
[Mh] Termos MeSH primário: Cinamatos/isolamento & purificação
Glicosídeos/isolamento & purificação
Heracleum/química
Extratos Vegetais/química
[Mh] Termos MeSH secundário: Células 3T3-L1
Adipócitos/efeitos dos fármacos
Adipogenia/efeitos dos fármacos
Animais
Glicosídeos Cardíacos
Cinamatos/química
Glicosídeos/química
Camundongos
Fenóis/química
Raízes de Plantas/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cardiac Glycosides); 0 (Cinnamates); 0 (Glycosides); 0 (Phenols); 0 (Plant Extracts); U14A832J8D (cinnamic acid)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170623
[St] Status:MEDLINE
[do] DOI:10.1080/14786419.2017.1340285


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[PMID]:29180011
[Au] Autor:Inoue N; Hirouchi T; Kasai A; Higashi S; Hiraki N; Tanaka S; Nakazawa T; Nunomura K; Lin B; Omori A; Hayata-Takano A; Kim YJ; Doi T; Baba A; Hashimoto H; Shintani N
[Ad] Endereço:Laboratory of Molecular Neuropharmacology, Graduate School of Pharmaceutical Sciences, Osaka University, 1-6 Yamadaoka, Suita, Osaka 565-0871, Japan; Interdisciplinary Program for Biomedical Sciences, Institute for Academic Initiatives, Osaka University, 1-1 Yamadaoka, Suita, Osaka 565-0871, Japan;
[Ti] Título:Unbiased compound screening with a reporter gene assay highlights the role of p13 in the cardiac cellular stress response.
[So] Source:Biochem Biophys Res Commun;495(2):1992-1997, 2018 01 08.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We recently showed that a 13-kDa protein (p13), the homolog protein of formation of mitochondrial complex V assembly factor 1 in yeast, acts as a potential protective factor in pancreatic islets under diabetes. Here, we aimed to identify known compounds regulating p13 mRNA expression to obtain therapeutic insight into the cellular stress response. A luciferase reporter system was developed using the putative promoter region of the human p13 gene. Overexpression of peroxisome proliferator-activated receptor gamma coactivator 1α, a master player regulating mitochondrial metabolism, increased both reporter activity and p13 expression. Following unbiased screening with 2320 known compounds in HeLa cells, 12 pharmacological agents (including 8 cardiotonics and 2 anthracyclines) that elicited >2-fold changes in p13 mRNA expression were identified. Among them, four cardiac glycosides decreased p13 expression and concomitantly elevated cellular oxidative stress. Additional database analyses showed highest p13 expression in heart, with typically decreased expression in cardiac disease. Accordingly, our results illustrate the usefulness of unbiased compound screening as a method for identifying novel functional roles of unfamiliar genes. Our findings also highlight the importance of p13 in the cellular stress response in heart.
[Mh] Termos MeSH primário: Glicosídeos Cardíacos/metabolismo
Avaliação Pré-Clínica de Medicamentos/métodos
Glicoproteínas/metabolismo
Ensaios de Triagem em Larga Escala/métodos
Chaperonas Moleculares/metabolismo
Miócitos Cardíacos/metabolismo
Estresse Oxidativo/fisiologia
Mapeamento de Interação de Proteínas/métodos
[Mh] Termos MeSH secundário: Genes Reporter
Células HeLa
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cardiac Glycosides); 0 (Glycoproteins); 0 (Molecular Chaperones); 0 (p13 glycoprotein, human)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE


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[PMID]:28618929
[Au] Autor:Kulkarni YM; Yakisich JS; Azad N; Venkatadri R; Kaushik V; O'Doherty G; Iyer AKV
[Ad] Endereço:1 Department of Pharmaceutical Sciences, School of Pharmacy, Hampton University, Hampton, VA, USA.
[Ti] Título:Anti-tumorigenic effects of a novel digitoxin derivative on both estrogen receptor-positive and triple-negative breast cancer cells.
[So] Source:Tumour Biol;39(6):1010428317705331, 2017 Jun.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:While there are targeted treatments for triple positive breast cancers, lack of specific biomarkers for triple-negative breast cancers (TNBC) has hindered the development of therapies for this subset of cancers. In this study, we evaluated the anticancer properties of cardiac glycoside Digitoxin (Dtx) and its synthetic analog MonoD on breast cancer cell lines MCF-7 (estrogen receptor-positive breast cancer) and MDA-MB-468 (triple-negative breast cancer). Both cardiac glycosides, at concentrations within the therapeutic range, increased the fraction of cells in the G /G phase of the cell cycle, decreased viability, and inhibited the migration of MCF-7 and MDA-MB-468 cells. Both cardiac glycosides increased production of superoxide and induced apoptosis in both cell types. Reduced protein levels of nuclear factor kappa B and IkappaB kinase-beta were found in cardiac glycoside-treated cells, indicating that the cellular effects of these compounds are mediated via nuclear factor kappa B pathway. This study demonstrates the cytotoxic potential of digitoxin, and more importantly its synthetic analog MonoD, in the treatment of triple-positive breast cancer and more importantly the aggressive triple-negative breast cancer. Collectively, this study provides a basis for the reevaluation of cardiac glycosides in the treatment of breast cancer and more importantly reveals their potential in the treatment of triple-negative breast cancers.
[Mh] Termos MeSH primário: Digitoxina/administração & dosagem
Receptores Estrogênicos/genética
Neoplasias de Mama Triplo Negativas/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Carcinogênese/genética
Glicosídeos Cardíacos/genética
Ciclo Celular/efeitos dos fármacos
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Digitoxina/análogos & derivados
Feminino
Seres Humanos
Células MCF-7
Camundongos
NF-kappa B/genética
Neoplasias de Mama Triplo Negativas/genética
Neoplasias de Mama Triplo Negativas/patologia
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cardiac Glycosides); 0 (NF-kappa B); 0 (Receptors, Estrogen); E90NZP2L9U (Digitoxin)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170718
[Lr] Data última revisão:
170718
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170617
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317705331


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[PMID]:28591151
[Au] Autor:Osman MH; Farrag E; Selim M; Osman MS; Hasanine A; Selim A
[Ad] Endereço:Faculty of Medicine, Zagazig University, Zagazig, Egypt.
[Ti] Título:Cardiac glycosides use and the risk and mortality of cancer; systematic review and meta-analysis of observational studies.
[So] Source:PLoS One;12(6):e0178611, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Cardiac glycosides (CGs) including digitalis, digoxin and digitoxin are used in the treatment of congestive heart failure and atrial fibrillation. Pre-clinical studies have investigated the anti-neoplastic properties of CGs since 1960s. Epidemiological studies concerning the association between CGs use and cancer risk yielded inconsistent results. We have performed a systematic review and meta-analysis to summarize the effects of CGs on cancer risk and mortality. METHODS: PubMed, Scopus, Cochrane library, Medline and Web of Knowledge were searched for identifying relevant studies. Summary relative risks (RR) and 95% confidence intervals (CI) were calculated using random-effects model. RESULTS: We included 14 case-control studies and 15 cohort studies published between 1976 and 2016 including 13 cancer types. Twenty-four studies reported the association between CGs and cancer risk and six reported the association between CGs and mortality of cancer patients. Using CGs was associated with a higher risk of breast cancer (RR = 1.330, 95% CI: 1.247-1.419). Subgroup analysis showed that using CGs increased the risk of ER+ve breast cancer but not ER-ve. Using CGs wasn't associated with prostate cancer risk (RR = 1.015, 95% CI: 0.868-1.87). However, CGs decreased the risk in long term users and showed a protective role in decreasing the risk of advanced stages. CGs use was associated with increased all-cause mortality (HR = 1.35, 95% CI: 1.248-1.46) but not cancer-specific mortality (HR = 1.075, 95% CI: 0.968-1.194). CONCLUSION: The anti-tumor activity of CGs observed in pre-clinical studies requires high concentrations which can't be normally tolerated in humans. However, the estrogen-like activity of CGs could be responsible for increasing the risk of certain types of tumors.
[Mh] Termos MeSH primário: Glicosídeos Cardíacos/efeitos adversos
Neoplasias/mortalidade
Estudos Observacionais como Assunto
[Mh] Termos MeSH secundário: Feminino
Seres Humanos
Masculino
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Nome de substância:
0 (Cardiac Glycosides)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170608
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0178611


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[PMID]:28430151
[Au] Autor:Felippe Gonçalves-de-Albuquerque C; Ribeiro Silva A; Ignácio da Silva C; Caire Castro-Faria-Neto H; Burth P
[Ad] Endereço:Laboratório de Imunofarmacologia, Instituto Oswaldo Cruz, FIOCRUZ, Rio de Janeiro RJ CEP 21040-900, Brazil. cassianofg@gmail.com.
[Ti] Título:Na/K Pump and Beyond: Na/K-ATPase as a Modulator of Apoptosis and Autophagy.
[So] Source:Molecules;22(4), 2017 Apr 21.
[Is] ISSN:1420-3049
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Lung cancer is a leading cause of global cancer deaths. Na/K-ATPase has been studied as a target for cancer treatment. Cardiotonic steroids (CS) trigger intracellular signalling upon binding to Na/K-ATPase. Normal lung and tumour cells frequently express different pump isoforms. Thus, Na/K-ATPase is a powerful target for lung cancer treatment. Drugs targeting Na/K-ATPase may induce apoptosis and autophagy in transformed cells. We argue that Na/K-ATPase has a role as a potential target in chemotherapy in lung cancer treatment. We discuss the effects of Na/K-ATPase ligands and molecular pathways inducing deleterious effects on lung cancer cells, especially those leading to apoptosis and autophagy.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Glicosídeos Cardíacos/farmacologia
Neoplasias Pulmonares/tratamento farmacológico
ATPase Trocadora de Sódio-Potássio/metabolismo
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/uso terapêutico
Apoptose/efeitos dos fármacos
Autofagia/efeitos dos fármacos
Glicosídeos Cardíacos/uso terapêutico
Seres Humanos
Neoplasias Pulmonares/enzimologia
Terapia de Alvo Molecular
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Cardiac Glycosides); EC 3.6.3.9 (Sodium-Potassium-Exchanging ATPase)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170606
[Lr] Data última revisão:
170606
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170422
[St] Status:MEDLINE


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[PMID]:28420099
[Au] Autor:Orlov SN; Klimanova EA; Tverskoi AM; Vladychenskaya EA; Smolyaninova LV; Lopina OD
[Ad] Endereço:Laboratory of Biological Membranes, Faculty of Biology, M.V. Lomonosov Moscow State University, 1/12 Leninskie Gory, Moscow 119234, Russia. sergeinorlov@yandex.ru.
[Ti] Título:Na⁺ ,K⁺ -Dependent and -Independent Signaling Triggered by Cardiotonic Steroids: Facts and Artifacts.
[So] Source:Molecules;22(4), 2017 Apr 14.
[Is] ISSN:1420-3049
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Na⁺,K⁺-ATPase is the only known receptor of cardiotonic steroids (CTS) whose interaction with catalytic α-subunits leads to inhibition of this enzyme. As predicted, CTS affect numerous cellular functions related to the maintenance of the transmembrane gradient of monovalent cations, such as electrical membrane potential, cell volume, transepithelial movement of salt and osmotically-obliged water, symport of Na⁺ with inorganic phosphate, glucose, amino acids, nucleotides, etc. During the last two decades, it was shown that side-by-side with these canonical Na⁺ /K⁺ -dependent cellular responses, long-term exposure to CTS affects transcription, translation, tight junction, cell adhesion and exhibits tissue-specific impact on cell survival and death. It was also shown that CTS trigger diverse signaling cascades via conformational transitions of the Na⁺,K⁺-ATPase α-subunit that, in turn, results in the activation of membrane-associated non-receptor tyrosine kinase Src, phosphatidylinositol 3-kinase and the inositol 1,4,5-triphosphate receptor. These findings allowed researchers to propose that endogenous CTS might be considered as a novel class of steroid hormones. We focus our review on the analysis of the relative impact Na⁺ ,K⁺ -mediated and -independent pathways in cellular responses evoked by CTS.
[Mh] Termos MeSH primário: Glicosídeos Cardíacos/farmacologia
Transdução de Sinais/efeitos dos fármacos
ATPase Trocadora de Sódio-Potássio/metabolismo
[Mh] Termos MeSH secundário: Animais
Glicosídeos Cardíacos/química
Adesão Celular/efeitos dos fármacos
Morte Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Regulação da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Bombas de Íon/metabolismo
Extratos Vegetais/química
Extratos Vegetais/farmacologia
ATPase Trocadora de Sódio-Potássio/química
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cardiac Glycosides); 0 (Ion Pumps); 0 (Plant Extracts); EC 3.6.3.9 (Sodium-Potassium-Exchanging ATPase)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170531
[Lr] Data última revisão:
170531
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170420
[St] Status:MEDLINE


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[PMID]:28388428
[Au] Autor:Cayo MA; Mallanna SK; Di Furio F; Jing R; Tolliver LB; Bures M; Urick A; Noto FK; Pashos EE; Greseth MD; Czarnecki M; Traktman P; Yang W; Morrisey EE; Grompe M; Rader DJ; Duncan SA
[Ad] Endereço:Department of Cell Biology, Neurobiology, and Anatomy, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226, USA.
[Ti] Título:A Drug Screen using Human iPSC-Derived Hepatocyte-like Cells Reveals Cardiac Glycosides as a Potential Treatment for Hypercholesterolemia.
[So] Source:Cell Stem Cell;20(4):478-489.e5, 2017 Apr 06.
[Is] ISSN:1875-9777
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Efforts to identify pharmaceuticals to treat heritable metabolic liver diseases have been hampered by the lack of models. However, cells with hepatocyte characteristics can be produced from induced pluripotent stem cells (iPSCs). Here, we have used hepatocyte-like cells generated from homozygous familial hypercholesterolemia (hoFH) iPSCs to identify drugs that can potentially be repurposed to lower serum LDL-C. We found that cardiac glycosides reduce the production of apolipoprotein B (apoB) from human hepatocytes in culture and the serum of avatar mice harboring humanized livers. The drugs act by increasing the turnover of apoB protein. Analyses of patient medical records revealed that the treatment of patients with cardiac glycosides reduced serum LDL-C levels. These studies highlight the effectiveness of using iPSCs to screen for potential treatments for inborn errors of hepatic metabolism and suggest that cardiac glycosides could provide an approach for reducing hepatocyte production of apoB and treating hypercholesterolemia.
[Mh] Termos MeSH primário: Glicosídeos Cardíacos/uso terapêutico
Avaliação Pré-Clínica de Medicamentos
Hepatócitos/citologia
Hipercolesterolemia/tratamento farmacológico
Células-Tronco Pluripotentes Induzidas/citologia
[Mh] Termos MeSH secundário: Animais
Apolipoproteínas B/metabolismo
Glicosídeos Cardíacos/farmacologia
LDL-Colesterol/sangue
Células Hep G2
Hepatócitos/efeitos dos fármacos
Hepatócitos/metabolismo
Homozigoto
Seres Humanos
Hipercolesterolemia/sangue
Hipolipemiantes/química
Hipolipemiantes/farmacologia
Hipolipemiantes/uso terapêutico
Células-Tronco Pluripotentes Induzidas/efeitos dos fármacos
Células-Tronco Pluripotentes Induzidas/metabolismo
Camundongos
Camundongos Endogâmicos NOD
Proteólise/efeitos dos fármacos
Bibliotecas de Moléculas Pequenas/farmacologia
Bibliotecas de Moléculas Pequenas/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apolipoproteins B); 0 (Cardiac Glycosides); 0 (Cholesterol, LDL); 0 (Hypolipidemic Agents); 0 (Small Molecule Libraries)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170731
[Lr] Data última revisão:
170731
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170408
[St] Status:MEDLINE


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[PMID]:28292827
[Au] Autor:Garofalo S; Grimaldi A; Chece G; Porzia A; Morrone S; Mainiero F; D'Alessandro G; Esposito V; Cortese B; Di Angelantonio S; Trettel F; Limatola C
[Ad] Endereço:Department of Physiology and Pharmacology.
[Ti] Título:The Glycoside Oleandrin Reduces Glioma Growth with Direct and Indirect Effects on Tumor Cells.
[So] Source:J Neurosci;37(14):3926-3939, 2017 Apr 05.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Oleandrin is a glycoside that inhibits the ubiquitous enzyme Na /K -ATPase. In addition to its known effects on cardiac muscle, recent and evidence highlighted its potential for anticancer properties. Here, we evaluated for the first time the effect of oleandrin on brain tumors. To this aim, mice were transplanted with human or murine glioma and analyzed for tumor progression upon oleandrin treatment. In both systems, oleandrin impaired glioma development, reduced tumor size, and inhibited cell proliferation. We demonstrated that oleandrin does the following: (1) enhances the brain-derived neurotrophic factor (BDNF) level in the brain; (2) reduces both microglia/macrophage infiltration and CD68 immunoreactivity in the tumor mass; (3) decreases astrogliosis in peritumoral area; and (4) reduces glioma cell infiltration in healthy parenchyma. In BDNF-deficient mice (bdnftm1Jae/J) and in glioma cells silenced for TrkB receptor expression, oleandrin was not effective, indicating a crucial role for BDNF in oleandrin's protective and antitumor functions. In addition, we found that oleandrin increases survival of temozolomide-treated mice. These results encourage the development of oleandrin as possible coadjuvant agent in clinical trials of glioma treatment. In this work, we paved the road for a new therapeutic approach for the treatment of brain tumors, demonstrating the potential of using the cardioactive glycoside oleandrin as a coadjuvant drug to standard chemotherapeutics such as temozolomide. In murine models of glioma, we demonstrated that oleandrin significantly increased mouse survival and reduced tumor growth both directly on tumor cells and indirectly by promoting an antitumor brain microenvironment with a key protective role played by the neurotrophin brain-derived neurotrophic factor.
[Mh] Termos MeSH primário: Neoplasias Encefálicas/tratamento farmacológico
Cardenolídeos/uso terapêutico
Glicosídeos Cardíacos/uso terapêutico
Glioma/tratamento farmacológico
Carga Tumoral/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Neoplasias Encefálicas/patologia
Cardenolídeos/farmacologia
Glicosídeos Cardíacos/farmacologia
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Sobrevivência Celular/fisiologia
Glioma/patologia
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos SCID
Camundongos Transgênicos
Carga Tumoral/fisiologia
Ensaios Antitumorais Modelo de Xenoenxerto/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cardenolides); 0 (Cardiac Glycosides); II95UDU7I4 (oleandrin)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170727
[Lr] Data última revisão:
170727
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170316
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.2296-16.2017


  9 / 2890 MEDLINE  
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[PMID]:28234008
[Au] Autor:Chen WL; Ren Y; Ren J; Erxleben C; Johnson ME; Gentile S; Kinghorn AD; Swanson SM; Burdette JE
[Ad] Endereço:Department of Medicinal Chemistry and Pharmacognosy, College of Pharmacy, University of Illinois at Chicago , Chicago, Illinois 60612, United States.
[Ti] Título:(+)-Strebloside-Induced Cytotoxicity in Ovarian Cancer Cells Is Mediated through Cardiac Glycoside Signaling Networks.
[So] Source:J Nat Prod;80(3):659-669, 2017 Mar 24.
[Is] ISSN:1520-6025
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:(+)-Strebloside, a cardiac glycoside isolated from the stem bark of Streblus asper collected in Vietnam, has shown some potential for further investigation as an antineoplastic agent. A mechanistic study using an in vitro assay and molecular docking analysis indicated that (+)-strebloside binds and inhibits Na /K -ATPase in a similar manner to digitoxin. Inhibition of growth of different high-grade serous ovarian cancer cells including OVCAR3, OVSAHO, Kuramochi, OVCAR4, OVCAR5, and OVCAR8 resulted from treatment with (+)-strebloside. Furthermore, this compound blocked cell cycle progression at the G2 phase and induced PARP cleavage, indicating apoptosis activation in OVCAR3 cells. (+)-Strebloside potently inhibited mutant p53 expression through the induction of ERK pathways and inhibited NF-κB activity in human ovarian cancer cells. However, in spite of its antitumor potential, the overall biological activity of (+)-strebloside must be regarded as being typical of better-known cardiac glycosides such as digoxin and ouabain. Further chemical alteration of cardiac glycosides might help to reduce negative side effects while increasing cancer cell cytotoxicity.
[Mh] Termos MeSH primário: Antineoplásicos Fitogênicos/isolamento & purificação
Antineoplásicos Fitogênicos/farmacologia
Glicosídeos Cardíacos/isolamento & purificação
Glicosídeos Cardíacos/farmacologia
ATPase Trocadora de Sódio-Potássio/antagonistas & inibidores
[Mh] Termos MeSH secundário: Antineoplásicos Fitogênicos/química
Apoptose/efeitos dos fármacos
Glicosídeos Cardíacos/química
Digoxina/farmacologia
Feminino
Células HT29
Seres Humanos
Estrutura Molecular
NF-kappa B/metabolismo
Neoplasias Epiteliais e Glandulares
Ouabaína/farmacologia
Neoplasias Ovarianas
Transdução de Sinais/efeitos dos fármacos
Estereoisomerismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Phytogenic); 0 (Cardiac Glycosides); 0 (NF-kappa B); 0 (strebloside-); 5ACL011P69 (Ouabain); 73K4184T59 (Digoxin); EC 3.6.3.9 (Sodium-Potassium-Exchanging ATPase)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170721
[Lr] Data última revisão:
170721
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170225
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jnatprod.6b01150


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[PMID]:28174828
[Au] Autor:Wassertheil-Smoller S; McGinn AP; Martin L; Rodriguez BL; Stefanick ML; Perez M
[Ti] Título:The Associations of Atrial Fibrillation With the Risks of Incident Invasive Breast and Colorectal Cancer.
[So] Source:Am J Epidemiol;185(5):372-384, 2017 Mar 01.
[Is] ISSN:1476-6256
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Atrial fibrillation (AF) is a common arrhythmia that poses a significant risk of stroke. Cross-sectional and case-control studies have shown evidence of associations between AF and breast or colorectal cancer, but there have been no longitudinal studies in which this has been assessed. We prospectively examined a cohort of 93,676 postmenopausal women enrolled in the Women's Health Initiative from 1994 to 1998 to determine whether there are relationships between baseline AF and the development of invasive breast or colorectal cancer. The prevalence of self-reported physician diagnosis of AF at baseline was 5.1%. Over approximately 15 years of follow-up, the incidence of invasive breast cancer was 5.7%, and the incidence of colorectal cancer was 1.6%. Adjusted hazard ratios and 95% confidence intervals were obtained using Cox proportional hazards models. We found no significant association between AF and incident colorectal cancer, but we did see a 19% excess risk of invasive breast cancer among those with AF (adjusted hazard ratio (HR) = 1.19, 95% confidence interval (CI): 1.03, 1.38). Additional adjustment for baseline use of cardiac glycosides attenuated the association between AF and invasive breast cancer (HR = 1.01, 95% CI: 0.85, 1.20). Cardiac glycoside use was strongly associated with incident invasive breast cancer (HR = 1.68, 95% CI: 1.33, 2.12) independent of AF and other confounders. Mechanisms of the associations among breast cancer, AF, and cardiac glycosides need further investigation.
[Mh] Termos MeSH primário: Fibrilação Atrial/epidemiologia
Neoplasias da Mama/epidemiologia
Glicosídeos Cardíacos/efeitos adversos
Neoplasias Colorretais/epidemiologia
[Mh] Termos MeSH secundário: Idoso
Antiarrítmicos/administração & dosagem
Antiarrítmicos/efeitos adversos
Fibrilação Atrial/tratamento farmacológico
Glicosídeos Cardíacos/administração & dosagem
Comorbidade
Feminino
Seres Humanos
Incidência
Meia-Idade
Modelos de Riscos Proporcionais
Estudos Prospectivos
Medição de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Arrhythmia Agents); 0 (Cardiac Glycosides)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170209
[St] Status:MEDLINE
[do] DOI:10.1093/aje/kww185



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