RESUMO
Gastric cancer represents a diffuse and aggressive neoplasm, whose mortality index is among the highest in the world. Predisposing factors are E-cadherin mutations, Helicobacter pylori infection, and a diet rich in salted and smoked food, with a low intake of fresh fruits and vegetables. Here, we analyzed the effect of total lipophilic extracts of two Southern Italy tomato varieties, San Marzano and Corbarino, on an in vitro model of gastric cancer, YCC-1, YCC-2 and YCC-3 cell lines, characterized by different aggressiveness. Our results showed a possible role of these two varieties of tomatoes against typical neoplastic features. The treatment with tomato extracts affected cancer cell ability to grow both in adherence and in semisolid medium, reducing also cell migration ability. No toxic effects were observed on non-tumoral cells. We found, on gastric cancer cell lines, effects on both cell cycle progression and apoptosis modulation. The extent of antineoplastic effects, however, did not seem to correlate with the carotenoid content and antioxidant activity of the two tomato varieties. Our data indicate that San Marzano and Corbarino intake might be further considered as nutritional support not only in cancer prevention, but also for cancer patient diet.
Assuntos
Antineoplásicos Fitogênicos/farmacologia , Antioxidantes/farmacologia , Carotenoides/farmacologia , Solanum lycopersicum/química , Neoplasias Gástricas/tratamento farmacológico , Antineoplásicos Fitogênicos/isolamento & purificação , Antioxidantes/isolamento & purificação , Apoptose/efeitos dos fármacos , Carotenoides/isolamento & purificação , Ciclo Celular/efeitos dos fármacos , Linhagem Celular Tumoral , Movimento Celular/efeitos dos fármacos , Proliferação de Células/efeitos dos fármacos , Relação Dose-Resposta a Droga , Frutas/química , Humanos , Itália , Invasividade Neoplásica , Fitoterapia , Plantas Medicinais , Neoplasias Gástricas/metabolismo , Neoplasias Gástricas/patologia , Fatores de TempoRESUMO
Obesity is characterized by a disruption in energy balance regulation that results in an excess accumulation of body fat. Its increasing prevalence poses a major public health concern because it is a risk factor for a host of additional chronic conditions, including type 2 diabetes, hypertension, and cardiovascular disease. Obesity is increasingly recognized as a growing cause of cancer risk. In particular excessive adipose expansion during obesity causes adipose dysfunction and inflammation that can regulate tumor growth. In obesity, dysregulated systemic metabolism and inflammation induce hyperinsulinemia, hyperglycemia, dyslipidemia, and enhance sex hormone production with increased secretion of proinflammatory adipokine that impact breast cancer development and progression. This review describes how adipose inflammation that characterizes obesity is responsible of microenvironment to promote cancer, and discuss how steroid hormones, that are essential for the maintenance of the normal development, growth and differentiation of the cells, influence the induction and progression of breast cancer. J. Cell. Physiol. 232: 69-77, 2017. © 2016 Wiley Periodicals, Inc.
Assuntos
Tecido Adiposo/metabolismo , Neoplasias da Mama/metabolismo , Diabetes Mellitus Tipo 2/metabolismo , Metabolismo Energético/fisiologia , Resistência à Insulina/fisiologia , Obesidade/metabolismo , Animais , Neoplasias da Mama/complicações , Neoplasias da Mama/genética , Diabetes Mellitus Tipo 2/complicações , Humanos , Obesidade/complicaçõesRESUMO
pRb2/p130 is a key tumor suppressor, whose oncosuppressive activity has mainly been attributed to its ability to negatively regulate cell cycle by interacting with the E2F4 and E2F5 transcription factors. Indeed, pRb2/p130 has been found altered in various cancer types in which it functions as a valuable prognostic marker. Here, we analyzed pRb2/p130 expression in gastric cancer tissue samples of diffuse histotype, in comparison with their normal counterparts. We found a cytoplasmic localization of pRb2/p130 in cancer tissue samples, whereas, in normal counterparts, we observed the expected nuclear localization. pRb2/p130 cytoplasmic delocalization can lead to cell cycle deregulation, but considering the emerging involvement of pRb2/p130 in other key cellular processes, it could contribute to gastric tumorigenesis also through other mechanisms. Our data support the necessity of further investigations to verify the possibility of using pRb2/p130 as a biomarker or potential therapeutic target for diffuse gastric cancer.
Assuntos
Proteína Substrato Associada a Crk/metabolismo , Citoplasma/metabolismo , Proteínas Salivares Ricas em Prolina/metabolismo , Neoplasias Gástricas/metabolismo , Fatores de Transcrição/metabolismo , Proteínas de Ciclo Celular/metabolismo , Divisão Celular/genética , Divisão Celular/fisiologia , Feminino , Genes Supressores de Tumor/fisiologia , Humanos , Masculino , Fosfoproteínas/fisiologia , Proteína do Retinoblastoma/metabolismo , Proteína p130 Retinoblastoma-Like/metabolismo , Neoplasias Gástricas/genéticaRESUMO
BACKGROUND/AIM: Self-efficacy for coping with cancer plays a critical role in influencing psychological cancer-related outcomes, some studies suggested its role in enhancing or reducing the effects of psychological interventions in cancer patients. Reiki has recently been included among the efficacious complementary therapeutic intervention for cancer patients. PATIENTS AND METHODS: The present study evaluated the role of self-efficacy for coping with cancer as buffer of the Reiki treatment effects on cancer-related symptoms in a randomized controlled trial (intervention versus control group) of breast cancer patients (N=110) during the pre-surgery phase. RESULTS: Results showed that self-efficacy for coping with cancer can influence the effect of a Reiki treatment. Higher efficacious patients showed a more powerful effect of the Reiki intervention on both anxiety and mood than the low efficacious patients. CONCLUSION: From a practical perspective, the study provides insightful results for healthcare professionals.