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1.
Mol Biol Rep ; 39(4): 4909-14, 2012 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-22143879

RESUMO

The astonishing development of broad genomics and proteomics tools have catalyzed a new era in both therapeutic interventions and nutrition in prostate cancer. The terms pharmacogenomics and nutrigenomics have been derived out of their genetic forbears as large-scale genomics technologies have been established in the last decade. It is unquestionable that rationale of both disciplines is to individualize or personalize medicine and food and nutrition, and eventually health, by tailoring the drug or the food to the individual genotype. The purpose of this review is to significantly inspect results from current research concerning the mechanisms of action of phytonutrients and potential effects on prostate cancer. Substantial emerging data supports the synergistic adiministration of nutraceuticals with TRAIL in prostate cancer progression to circumvent TRAIL refractoriness. Nonetheless, developing novel scientific methods for discovery, validation, characterization and standardization of these multicomponent phyto-therapeutics is vital to their recognition into mainstream medicine. The key to interpret a personalized response is a greater comprehension of nutrigenomics, proteomics and metabolomics.


Assuntos
Suplementos Nutricionais , Nutrigenômica , Neoplasias da Próstata/tratamento farmacológico , Ligante Indutor de Apoptose Relacionado a TNF/uso terapêutico , Humanos , Masculino , Modelos Biológicos , Ligante Indutor de Apoptose Relacionado a TNF/farmacologia
2.
Immunogenetics ; 63(12): 773-87, 2011 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-21932052

RESUMO

Transient receptor potential (TRP) channels belong to a large family of cation channels and are the "border guards" predominantly localized to the plasma membrane. Research over the years has considerably and highly developed the knowledge of expression and functional aspects of the TRPM channels. A closer look at the channel dynamics has dismantled undeniable substantiation for multifaceted roles for TRPM channel-mediated extracellular Ca(2+) influx in several physiological and pathophysiological functions. Given the wealth of literature unfolding the multiple roles of TRP channels in physiology in a very extensive range of different mammalian tissues, this review confines itself to the literature describing the multiple roles of TRPM channels in diabetes, smooth muscle cell regulation, immunological responses, and emerging aspects of cancer. We also focus on differential activities of TRPM channels after post-transcriptional and post-translational processing and their exquisite roles at various cellular and molecular levels.


Assuntos
Fenômenos Imunogenéticos , Canais de Cátion TRPM/genética , Canais de Cátion TRPM/metabolismo , Animais , Membrana Celular/metabolismo , Diabetes Mellitus/metabolismo , Humanos , Melanócitos/metabolismo , Camundongos , Miócitos de Músculo Liso/metabolismo , Neoplasias/metabolismo , Processamento de Proteína Pós-Traducional , Processamento Pós-Transcricional do RNA
3.
Tumour Biol ; 32(6): 1057-70, 2011 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-21769672

RESUMO

PDGF is a growth factor and is extensively involved in multi-dimensional cellular dynamics. It switches on a plethora of molecules other than its classical pathway. It is engaged in various transitions of development; however, if the unleashed potentials lead astray, it brings forth tumourigenesis. Conventionally, it has been assumed that the components of this signalling pathway show fidelity and act with a high degree of autonomy. However, as illustrated by the PDGF signal transduction, reinterpretation of recent data suggests that machinery is often shared between multiple pathways, and other components crosstalk to each other through multiple mechanisms. It is important to note that metastatic cascade is an intricate process that we have only begun to understand in recent years. Many of the early steps of this PDGF cascade are not readily targetable in the clinic. In this review, we will unravel the paradoxes with reference to mitrons and cellular plasticity and discuss how disruption of signalling cascade triggers cellular proliferation phase transition and metastasis. We will also focus on the therapeutic interventions to counteract resultant molecular disorders.


Assuntos
Fator de Crescimento Derivado de Plaquetas/metabolismo , Receptor alfa de Fator de Crescimento Derivado de Plaquetas/metabolismo , Receptor beta de Fator de Crescimento Derivado de Plaquetas/metabolismo , Transdução de Sinais , Humanos , Modelos Biológicos , Neoplasias/metabolismo , Neoplasias/patologia , Fosforilação , Ligação Proteica , Isoformas de Proteínas/metabolismo
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