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[PMID]:29314795
[Au] Autor:Konic-Ristic A; Stanojkovic T; Srdic-Rajic T; Dilber S; Dordevic B; Stankovic I; Juranic Z
[Ti] Título:In vitro assessment of antiproliferative action selectivity of dietary isothiocyanates for tumor versus normal human cells.
[So] Source:Vojnosanit Pregl;73(7):636-42, 2016 Jul.
[Is] ISSN:0042-8450
[Cp] País de publicação:Serbia
[La] Idioma:eng
[Ab] Resumo:Background/Aim: Numerous epidemiological studies have shown beneficial effects of cruciferous vegetables consumption in cancer chemoprevention. Biologically active compounds of different Brassicaceae species with antitumor potential are isothiocyanates, present in the form of their precursors - glucosinolates. The aim of this study was to determine the selectivity of antiproliferative action of dietary isothiocyanates for malignant versus normal cells. Methods: Antiproliferative activity of three isothiocyanates abundant in human diet: sulforaphane, benzyl isothiocyanate (BITC) and phenylethyl isothiocyanate, on human cervix carcinoma cell line - HeLa, melanoma cell line - Fem-x, and colon cancer cell line - LS 174, and on peripheral blood mononuclear cells (PBMC), with or without mitogen, were determined by MTT colorimetric assay 72 h after their continuous action. Results: All investigated isothiocyanates inhibited the proliferation of HeLa, Fem-x and LS 174 cells. On all cell lines treated, BITC was the most potent inhibitor of cell proliferation with half-maximum inhibitory concentration (IC50) values of 5.04 mmoL m-3 on HeLa cells, 2.76 mmol m-3 on Fem-x, and 14.30 mmol m-3 on LS 174 cells. Antiproliferative effects on human PBMC were with higher IC50 than on malignant cells. Indexes of selectivity, calculated as a ratio between IC50 values obtained on PBMC and malignant cells, were between 1.12 and 16.57, with the highest values obtained for the action of BITC on melanoma Fem-x cells. Conclusion: Based on its antiproliferative effects on malignant cells, as well as the selectivity of the action to malignant vs normal cells, benzyl isothiocyanate can be considered as a promising candidate in cancer chemoprevention. In general, the safety of investigated compounds, in addition to their antitumor potential, should be considered as an important criterion in cancer chemoprevention. Screening of selectivity is a plausible approach to the evaluation of safety of both natural isothiocyanates and synthesised analogues of these bioactive compounds.
[Mh] Termos MeSH primário: Anticarcinógenos/farmacologia
Proliferação Celular/efeitos dos fármacos
Dieta
Isotiocianatos/farmacologia
Neoplasias/prevenção & controle
[Mh] Termos MeSH secundário: Sobrevivência Celular/efeitos dos fármacos
Células HeLa
Seres Humanos
Leucócitos Mononucleares/citologia
Leucócitos Mononucleares/efeitos dos fármacos
Neoplasias/patologia
Células Tumorais Cultivadas
Verduras/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticarcinogenic Agents); 0 (Isothiocyanates)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180110
[St] Status:MEDLINE
[do] DOI:10.2298/VSP141103066K


  2 / 9551 MEDLINE  
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[PMID]:29225112
[Au] Autor:Kashyap D; Sharma A; Sak K; Tuli HS; Buttar HS; Bishayee A
[Ad] Endereço:Department of Histopathology, Postgraduate Institute of Medical Education and Research, Chandigarh 160 012, Punjab, India.
[Ti] Título:Fisetin: A bioactive phytochemical with potential for cancer prevention and pharmacotherapy.
[So] Source:Life Sci;194:75-87, 2018 Feb 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:A wide variety of chronic diseases, such as neurodegenerative and cardiovascular disorders, diabetes mellitus, osteoarthtitis, obesity and various cancers, are now being treated with cost effective phytomedicines. Since synthetic medicines are very expensive, concerted efforts are being made in developing and poor countries to discover cost effective medicines for the treatment of non-communicable diseases (NCDs). Understanding the underlying mechanisms of bioactive medicines from natural sources would not only open incipient avenues for the scientific community and pharmaceutical industry to discover new drug molecules for the therapy of NCDs, but also help to garner knowledge for alternative therapeutic approaches for the management of chronic diseases. Fisetin is a polyphenolic molecule of flavonoids class, and belongs to the bioactive phytochemicals that have potential to block multiple signaling pathways associated with NCDs such as cell division, angiogenesis, metastasis, oxidative stress, and inflammation. The emerging evidence suggests that fisetin may be useful for the prevention and management of several types of human malignancies. Efforts are being made to enhance the bioavailability of fisetin after oral administration to prevent and/or treat cancer of the liver, breast, ovary and other organs. The intent of this review is to highlight the in vitro and in vivo activities of fisetin and to provide up-to-date information about the molecular interactions of fisetin with its cellular targets involved in cancer initiation, promotion and progression as well as to focus on strategies underway to increase the bioavailability and reduce the risk of deleterious effects, if any, associated with fisetin administration.
[Mh] Termos MeSH primário: Anti-Inflamatórios/uso terapêutico
Anticarcinógenos/uso terapêutico
Antioxidantes/uso terapêutico
Flavonoides/uso terapêutico
Neoplasias/prevenção & controle
Compostos Fitoquímicos/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios/química
Anti-Inflamatórios/farmacologia
Anticarcinógenos/química
Anticarcinógenos/farmacologia
Antioxidantes/química
Antioxidantes/farmacologia
Apoptose/efeitos dos fármacos
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Flavonoides/química
Flavonoides/farmacologia
Seres Humanos
Neoplasias/metabolismo
Compostos Fitoquímicos/química
Compostos Fitoquímicos/farmacologia
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Anticarcinogenic Agents); 0 (Antioxidants); 0 (Flavonoids); 0 (Phytochemicals); OO2ABO9578 (fisetin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE


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[PMID]:29190630
[Au] Autor:Chen CM; Hsieh SC; Lin CL; Lin YS; Tsai JP; Hsieh YH
[Ad] Endereço:Division of Neurosurgery, Department of Surgery, Changhua Christian Hospital, Changhua, Taiwan.
[Ti] Título:Alpha-Mangostin Suppresses the Metastasis of Human Renal Carcinoma Cells by Targeting MEK/ERK Expression and MMP-9 Transcription Activity.
[So] Source:Cell Physiol Biochem;44(4):1460-1470, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: α-mangostin has anti-carcinogenic effects against several cancers. We investigated the molecular mechanism of this compound on the metastasis of human renal carcinoma cells. METHODS: Cell viability was measured using the MTT assay, and cell cycle distribution using flow cytometry. A Matrigel-based assay was used to measure in vitro cell migration and invasion. MAPK-related proteins and matrix metalloproteinase (MMP)-9 and MMP-2 expression were measured by western blotting, and MMP2/-9 activities were determined by gelatin zymography. RT-qPCR and a luciferase assay were used to examine the transcriptional activity of MMP-9. RESULTS: α-mangostin inhibited the migration and invasion of RCC cells in a dose-dependent manner, but had no evident cytotoxic effects. Treatment of 786-O cells with α-mangostin inhibited activation of MEK and ERK. Treatment with a specific MEK inhibitor (U0126) enhanced the inhibitory effects of α-mangostin on cell migration and invasion, and the phosphorylation of ERK and MEK. Moreover, α-mangostin inhibited the expression of the MMP-9 mRNA levels as well as the activity of MMP-9 promoter, and these suppressive effects were further enhanced by U0126. CONCLUSIONS: Our results suggest that α-mangostin suppresses cell migration and invasion via MEK/ERK/MMP9 pathway, and might be a promising anti-metastatic agent against human renal cell carcinoma.
[Mh] Termos MeSH primário: Anticarcinógenos/toxicidade
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
MAP Quinase Quinase Quinases/metabolismo
Metaloproteinase 9 da Matriz/metabolismo
Transdução de Sinais/efeitos dos fármacos
Transcrição Genética/efeitos dos fármacos
Xantonas/toxicidade
[Mh] Termos MeSH secundário: Anticarcinógenos/química
Butadienos/farmacologia
Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Seres Humanos
Neoplasias Renais/metabolismo
Neoplasias Renais/patologia
Metaloproteinase 2 da Matriz/metabolismo
Metaloproteinase 9 da Matriz/genética
Nitrilos/farmacologia
Xantonas/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticarcinogenic Agents); 0 (Butadienes); 0 (Nitriles); 0 (U 0126); 0 (Xanthones); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); EC 2.7.11.25 (MAP Kinase Kinase Kinases); EC 3.4.24.24 (Matrix Metalloproteinase 2); EC 3.4.24.35 (Matrix Metalloproteinase 9); U6RIV93RU1 (mangostin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE
[do] DOI:10.1159/000485582


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[PMID]:29267377
[Au] Autor:Paul B; Royston KJ; Li Y; Stoll ML; Skibola CF; Wilson LS; Barnes S; Morrow CD; Tollefsbol TO
[Ad] Endereço:Department of Biology, University of Alabama at Birmingham, Birmingham, Alabama, United States of America.
[Ti] Título:Impact of genistein on the gut microbiome of humanized mice and its role in breast tumor inhibition.
[So] Source:PLoS One;12(12):e0189756, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Since dietary polyphenols can have beneficial effects in prevention and treatment of cancer, we tested the hypothesis that breast cancer patients' intestinal microbiota is modulated by genistein (GE), an isoflavone found in soy, and that microbial alterations may offset the side effects brought about by chemotherapy. We demonstrated successful humanization of germ-free mice by transplanting fecal samples from breast cancer patients before and after chemotherapy. Mice were then grouped based on chemotherapy status and GE or control diet. We did not find any significant differences between pre-chemotherapy and post-chemotherapy bacterial composition and abundances. Germ-free mice on a GE diet showed differences in microbial composition as compared to mice on control diet. Four weeks after introduction of the customized GE diet, there was distinct clustering of GE-fed mice as compared to the control-fed group. In the gut microbiome of GE-treated humanized mice, there was an increase in abundance of genera Lactococcus and Eubacterium. Phylum Verrucomicrobia showed statistically significant (p = 0.02) differences in abundances between the GE-fed and control-fed groups. There was an increase in bacteria belonging to family Lachnospiraceae and Ruminococcaceae in GE-fed mice. Marked changes were observed in GE catabolism in mice humanized with fecal material from two of three patients' post-chemotherapy with complete disappearance of 4-ethylphenol and 2-(4-hydroxyphenol) propionic acid conjugates. The post-tumor samples did not show any distinct clustering of the gut microbiota between the two diet groups. There was an increase in latency of about 25% for tumor growth of the humanized mice that were on a GE diet as compared to humanized mice on a control diet. The average tumor size for the GE group was significantly decreased compared to the non-GE group. Collectively, our results suggest that the intestinal microbiota becomes altered with a GE diet before induction of tumor. Our findings indicate that GE modulates the microbiome in humanized mice that may contribute to its effects on increasing the latency of breast tumor and reducing tumor growth.
[Mh] Termos MeSH primário: Anticarcinógenos/farmacologia
Neoplasias da Mama/prevenção & controle
Modelos Animais de Doenças
Microbioma Gastrointestinal/efeitos dos fármacos
Genisteína/farmacologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Animais
Antineoplásicos/uso terapêutico
Neoplasias da Mama/tratamento farmacológico
Fezes/microbiologia
Feminino
Seres Humanos
Camundongos
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Anticarcinogenic Agents); 0 (Antineoplastic Agents); DH2M523P0H (Genistein)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189756


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[PMID]:29277760
[Au] Autor:Glei M; Fischer S; Lamberty J; Ludwig D; Lorkowski S; Schlörmann W
[Ad] Endereço:Friedrich Schiller University Jena, Institute of Nutrition, Department of Nutritional Toxicology, Jena, Germany.
[Ti] Título:Chemopreventive Potential of Fermented Raw and Roasted Hazelnuts in LT97 Colon Adenoma Cells.
[So] Source:Anticancer Res;38(1):83-93, 2018 01.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: Due to their unique composition of health-promoting compounds, the consumption of hazelnuts may contribute to the prevention of colon cancer. MATERIALS AND METHODS: Since hazelnuts are often consumed roasted, the impact of different roasting conditions (RC1=140.6°C/25 min, RC2=155.1°C/20 min and RC3=180.4°C/21 min) on chemopreventive effects of in vitro fermented hazelnuts was analyzed in LT97 colon adenoma cells. RESULTS: FS (2.5%) of raw and roasted hazelnuts reduced H O -induced DNA damage while 5% FS significantly induced gene expression of SOD2 (3.0-fold) and GSTP1 (2.1-fold). GPx1 mRNA levels were significantly decreased (0.6-fold) by FS (2.5%). The growth of LT97 cells was significantly reduced by hazelnut FS in a time- and dose-dependent manner. Hazelnut FS (5%) increased the numbers of early apoptotic cells (9.6% on average) and caspase-3 activities (6.4-fold on average). CONCLUSION: These results indicate a chemopreventive potential of in vitro fermented hazelnuts which is largely unaffected by the roasting process.
[Mh] Termos MeSH primário: Adenoma/tratamento farmacológico
Anticarcinógenos/farmacologia
Antineoplásicos/farmacologia
Neoplasias do Colo/tratamento farmacológico
Corylus
Preparações de Plantas/farmacologia
[Mh] Termos MeSH secundário: Adenoma/genética
Adenoma/prevenção & controle
Apoptose/efeitos dos fármacos
Catalase/genética
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Neoplasias do Colo/genética
Neoplasias do Colo/prevenção & controle
Culinária
Dano ao DNA/efeitos dos fármacos
Glutationa Peroxidase/genética
Glutationa S-Transferase pi/genética
Seres Humanos
Peróxido de Hidrogênio/toxicidade
Nozes
RNA Mensageiro/metabolismo
Superóxido Dismutase-1/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticarcinogenic Agents); 0 (Antineoplastic Agents); 0 (Plant Preparations); 0 (RNA, Messenger); 0 (SOD1 protein, human); BBX060AN9V (Hydrogen Peroxide); EC 1.11.1.- (glutathione peroxidase GPX1); EC 1.11.1.6 (Catalase); EC 1.11.1.9 (Glutathione Peroxidase); EC 1.15.1.1 (Superoxide Dismutase-1); EC 2.5.1.18 (GSTP1 protein, human); EC 2.5.1.18 (Glutathione S-Transferase pi)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180104
[Lr] Data última revisão:
180104
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171227
[St] Status:MEDLINE


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[PMID]:29277755
[Au] Autor:Radin DP; Krebs A; Maqsudlu A; Patel P
[Ad] Endereço:Department of Pharmacology, Stony Brook University School of Medicine, Stony Brook, NY, U.S.A. danradin1@gmail.com.
[Ti] Título:Our ACE in the HOLE: Justifying the Use of Angiotensin-converting Enzyme Inhibitors as Adjuvants to Standard Chemotherapy.
[So] Source:Anticancer Res;38(1):45-49, 2018 01.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Angiotensin-I-converting enzyme (ACE) inhibitors have been very effective in treating cardiac hypertension since their clinical inception over four decades ago. Since then, it has been established that angiotensin II, the product of ACE, has oncogenic and pro-proliferative qualities, which begs the question as to whether ACE inhibitors may have oncolytic characteristics. In fact, scattered reports suggest that ACE inhibitors are oncolytic and oncopreventive, but the available literature has yet to be thoroughly examined. In the present review, we examine the available literature and determine that ACE inhibitors would have great utility in the prevention and treatment of cancer. At the same time, they would augment the efficacy of chemo- and radiotherapy as well as mitigating damage to healthy tissue by standard chemotherapeutic regimens. We review some of the mounting clinical evidence and show that ACE inhibitors have oncolytic activity in multiple types of cancer and discuss the ability of ACE inhibitors to prevent cardiotoxicity of multiple chemotherapies. Our analysis demonstrates that the actions of ACE inhibitors converge on vascular endolthelial growth factor to reduce its levels in tumors and prevent construction of blood vessels to masses, leaving them nutrient-depleted and subsequently hindering their growth. Given that ACE inhibitors are approved by the Federal Drug Administration and the therapeutic dose for hypertension treatment also slows the growth of multiple cancers types, ACE inhibitors are in a perfect position to be repurposed as oncolytic agents, that would widely increase their utility in the clinic.
[Mh] Termos MeSH primário: Inibidores da Enzima Conversora de Angiotensina/uso terapêutico
Anticarcinógenos/uso terapêutico
Anti-Hipertensivos/uso terapêutico
Antineoplásicos/uso terapêutico
Neoplasias/tratamento farmacológico
Neoplasias/prevenção & controle
[Mh] Termos MeSH secundário: Animais
Cardiotônicos/uso terapêutico
Quimioterapia Adjuvante
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Angiotensin-Converting Enzyme Inhibitors); 0 (Anticarcinogenic Agents); 0 (Antihypertensive Agents); 0 (Antineoplastic Agents); 0 (Cardiotonic Agents)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180104
[Lr] Data última revisão:
180104
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171227
[St] Status:MEDLINE


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[PMID]:29113871
[Au] Autor:Chikara S; Nagaprashantha LD; Singhal J; Horne D; Awasthi S; Singhal SS
[Ad] Endereço:Department of Medical Oncology, Beckman Research Institute of City of Hope, Comprehensive Cancer Center and National Medical Center, Duarte, CA 91010, USA.
[Ti] Título:Oxidative stress and dietary phytochemicals: Role in cancer chemoprevention and treatment.
[So] Source:Cancer Lett;413:122-134, 2018 Jan 28.
[Is] ISSN:1872-7980
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Several epidemiological observations have shown an inverse relation between consumption of plant-based foods, rich in phytochemicals, and incidence of cancer. Phytochemicals, secondary plant metabolites, via their antioxidant property play a key role in cancer chemoprevention by suppressing oxidative stress-induced DNA damage. In addition, they modulate several oxidative stress-mediated signaling pathways through their anti-oxidant effects, and ultimately protect cells from undergoing molecular changes that trigger carcinogenesis. In several instances, however, the pro-oxidant property of these phytochemicals has been observed with respect to cancer treatment. Further, in vitro and in vivo studies show that several phytochemicals potentiate the efficacy of chemotherapeutic agents by exacerbating oxidative stress in cancer cells. Therefore, we reviewed multiple studies investigating the role of dietary phytochemicals such as, curcumin (turmeric), epigallocatechin gallate (EGCG; green tea), resveratrol (grapes), phenethyl isothiocyanate (PEITC), sulforaphane (cruciferous vegetables), hesperidin, quercetin and 2'-hydroxyflavanone (2HF; citrus fruits) in regulating oxidative stress and associated signaling pathways in the context of cancer chemoprevention and treatment.
[Mh] Termos MeSH primário: Anticarcinógenos/uso terapêutico
Antineoplásicos Fitogênicos/uso terapêutico
Antioxidantes/uso terapêutico
Dieta
Neoplasias/prevenção & controle
Estresse Oxidativo/efeitos dos fármacos
Compostos Fitoquímicos/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Resistência a Medicamentos Antineoplásicos
Seres Humanos
Neoplasias/metabolismo
Neoplasias/patologia
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anticarcinogenic Agents); 0 (Antineoplastic Agents, Phytogenic); 0 (Antioxidants); 0 (Phytochemicals)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171204
[Lr] Data última revisão:
171204
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171109
[St] Status:MEDLINE


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[PMID]:29107114
[Au] Autor:Sklirou A; Papanagnou ED; Fokialakis N; Trougakos IP
[Ad] Endereço:Department of Cell Biology and Biophysics, Faculty of Biology, National and Kapodistrian University of Athens, Athens 15784, Greece.
[Ti] Título:Cancer chemoprevention via activation of proteostatic modules.
[So] Source:Cancer Lett;413:110-121, 2018 Jan 28.
[Is] ISSN:1872-7980
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Proteins carry out the majority of cellular functions and maintain cellular homeodynamics mostly by participating in multimeric assemblies that operate as protein machines. Proteome quality control is thus critical for cellular functionality, and it is carried out through the curating activity of the proteostasis network (PN). Key components of the PN are the protein synthesis and trafficking modules, the endoplasmic reticulum unfolded protein response, molecular chaperones, and the two main degradation machineries, namely the ubiquitin proteasome and autophagy lysosome pathways. Part of the PN are also several stress responsive pathways, including nuclear factor erythroid 2-related factor 2 (Nrf2), which mobilises genomic responses against oxidative and/or xenobiotic damage. Nevertheless, the gradual accumulation of stressors during ageing or earlier due to lifestyle results in an increasingly damaged and unstable proteome. This outcome may then increase genomic instability due to reduced DNA replication fidelity or repair, leading to various age-related diseases such as cancer. Considering that the activation of proteostatic modules exerts anti-ageing effects in model organisms, we present herein a synopsis of studies showing that proteostatic modules activation (e.g. by natural products) represents a promising tumour-chemopreventive approach.
[Mh] Termos MeSH primário: Anticarcinógenos/uso terapêutico
Transformação Celular Neoplásica/efeitos dos fármacos
Neoplasias/prevenção & controle
Proteoma/efeitos dos fármacos
Proteostase/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Proliferação Celular/efeitos dos fármacos
Transformação Celular Neoplásica/genética
Transformação Celular Neoplásica/metabolismo
Transformação Celular Neoplásica/patologia
Senescência Celular/efeitos dos fármacos
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Neoplasias/genética
Neoplasias/metabolismo
Neoplasias/patologia
Estabilidade Proteica
Proteólise
Proteoma/genética
Proteoma/metabolismo
Proteostase/genética
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anticarcinogenic Agents); 0 (Proteome)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171204
[Lr] Data última revisão:
171204
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171107
[St] Status:MEDLINE


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[PMID]:29061805
[Au] Autor:Ma YS; Hsiao YT; Lin JJ; Liao CL; Lin CC; Chung JG
[Ad] Endereço:School of Chinese Medicine for Post-Baccalaureate, I-Shou University, Kaohsiung, Taiwan, R.O.C.
[Ti] Título:Phenethyl Isothiocyanate (PEITC) and Benzyl Isothiocyanate (BITC) Inhibit Human Melanoma A375.S2 Cell Migration and Invasion by Affecting MAPK Signaling Pathway .
[So] Source:Anticancer Res;37(11):6223-6234, 2017 11.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: Numerous evidence has shown that PEITC and BITC inhibit cancer cell migration and invasion. In this study, we investigated the anti-metastatic mechanisms of PEITC and BITC in human melanoma cancer A375.S2 cells in vitro. MATERIALS AND METHODS: We used a cell viability assay, an in-vitro scratch wound healing assay, a transwell assay for cell migration and invasion, a gelatin zymography assay, western blotting and EMSA to examine the anti-metastatic mechanisms of PEITC and BITC in A375.S2 cells. RESULTS: Sublethal concentrations of PEITC (0, 1, 2 and 2.5 µM) and BITC (0, 0.5, 1 and 2 µM) inhibited mobility, migration and invasion of A375.S2 cells that were assayed by wound healing and Transwell filter. PEITC and BITC inhibited MMP-2 activity in A375.S2 cells, as assessed by gelatin zymography assay. Results from western blotting indicated that PEITC (2.5 µM) and BITC (2 µM) decreased the levels of p-p38 following 24 and 48 h treatment. PEITC (1-2.5 µM) reduced the levels of p-JNK1/2 proteins following 48-h treatment but BITC increased p-JNK1/2 levels following 24-h treatment. PEITC (2.5 µM) reduced the levels of p-ERK1/2 proteins following 48-h treatment but BITC (0.5-2 µM) increased p-ERK1/2 levels following 24- and 48-h treatment. PEITC and BITC affect cell migration and invasion of A375.S2 cells via MAPK pathway. PEITC and BITC inhibited MMP-2 activity. PEITC increased NF-κB expression but BITC decreased NF-κB expression in the nucleus. Furthermore, NF-κB p65 binding to DNA was decreased following 2.5 µM PEITC treatment, but increased following treatment with 1-2 µM. However, 0.5-2 µM BITC treatment decreased the binding of NF-κB to DNA in A375.S2 cells, as assessed by electrophoretic mobility shift (EMSA) assay. CONCLUSION: Based on these observations, we suggest that PEITC and BITC can be used as anti-metastastic agents of human melanoma cells in the future.
[Mh] Termos MeSH primário: Anticarcinógenos/farmacologia
Movimento Celular/efeitos dos fármacos
Isotiocianatos/farmacologia
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Melanoma/patologia
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Técnicas In Vitro
Melanoma/tratamento farmacológico
Melanoma/metabolismo
NF-kappa B/metabolismo
Invasividade Neoplásica
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticarcinogenic Agents); 0 (Isothiocyanates); 0 (NF-kappa B); 6U7TFK75KV (phenethyl isothiocyanate); 871J6YOR8Q (benzyl isothiocyanate)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171025
[St] Status:MEDLINE


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[PMID]:29041990
[Au] Autor:Du M; Zhang Z; Gao T
[Ad] Endereço:Department of Dermatology, The Second Affiliated Hospital of Chongqing Medical University, 76 Linjiang Road, Yuzhong District, Chongqing, 400010, China. motaodu@163.com.
[Ti] Título:Piceatannol induced apoptosis through up-regulation of microRNA-181a in melanoma cells.
[So] Source:Biol Res;50(1):36, 2017 Oct 17.
[Is] ISSN:0717-6287
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Melanoma took top position among the lethal cancers and, despite there have been some great attempts made to increase the natural life of patients with metastatic disease, long-lasting and complete remissions are few. Piceatannol, owns the similar function as resveratrol, has been defined as an anti-cancer agent playing important role in inhibition of proliferation, migration and metastasis in various cancer. Thus, we aim to investigate the anti-cancer effect and mechanisms of piceatannol in melanoma cells. METHODS: Melanoma cell lines WM266-4 and A2058 were treated either with or without piceatannol. Cell viability and cell apoptosis were assessed by using MTT and Annexin V/PI assay, respectively. Cells were transfected with specific miRNA using Lipfectamine 2000. miRNA bingding ability to 3'-UTR region within specific gene was assed by firefly luciferase analysis. Gene and protein expression was eveluated by qRT-PCR and western blot analysis, respectively. RESULTS: Our study showed that piceatannol inhibited WM266-4 and A2058 cells growth and induced apoptosis. Totally, 16 differentially expressed miRNAs were screened out including 8 up-regulated and 8 down-regulated miRNAs. Expression level of miR-181a is significantly higher in piceatannol-treated cells than normal control and is lower in melanoma cancer tissues than its adjacent normal tissues. Bcl-2 is a target gene of miR-181a. Moreover, silencing of miR-181a reverses the decrease of cell viability induced by piceatannol in WM266-4 and A2058 cells. Taken together, present study uncovered the ability of piceatannol to repress melanoma cell growth and clarified the contribution of miR-181a in the anticancer role of piceatannol. CONCLUSION: The present study proposes that piceatannol can be taken into account to be a hopeful anticancer agent for melanoma.
[Mh] Termos MeSH primário: Anticarcinógenos/farmacologia
Apoptose/efeitos dos fármacos
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Melanoma/tratamento farmacológico
MicroRNAs/efeitos dos fármacos
Estilbenos/farmacologia
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Sobrevivência Celular
Seres Humanos
Melanoma/metabolismo
Melanoma/patologia
MicroRNAs/metabolismo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticarcinogenic Agents); 0 (MIRN-181 microRNA, human); 0 (MicroRNAs); 0 (Stilbenes); 6KS3LS0D4F (3,3',4,5'-tetrahydroxystilbene)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171019
[St] Status:MEDLINE
[do] DOI:10.1186/s40659-017-0141-8



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