Publicação
Overeating yeast display fatty acid-induced necrotic cell death
| Resumo: | [Excerpt] Cellular plasticity enables profound changes in cell phenotypes governed by tightly orchestrated interplay among distinct functional classes of regulatory molecules. This process typically involves the control of specific gene expression programs with distinct functional impacts on cellular behavior. One such manifestation of remarkable cellular plasticity— epithelial-mesenchymal transition (EMT)—has recently attracted broad interest in the field of cancer research, nearly 30 years after the pioneering work by Elizabeth Hay.1 EMT is a cell phenotype conversion utilized in tissue remodeling during embryonic development, re-enacted in adult tissue homeostasis (e.g. during regeneration upon injury) and in pathological conditions such as development of invasive and metastatic carcinomas or in fibrotic processes affecting vital organs such as the kidney or lungs.2,3 Cancer EMT has been recently demonstrated to generate breast carcinoma cancer stem-cells (CSCs) characterized by mesenchymal markers and by the capacity of self-renewal and of initiating secondary tumorigenesis.4 In addition, the process of EMT involves regulatory molecules (e.g., transcription factors Snail, Slug) that confer resistance to therapeutic induction of cell death. [...] |
|---|---|
| Autores principais: | Ludovico, Paula |
| Assunto: | Apoptosis Fatty Acids Homeostasis Humans Lipid Metabolism Mutation Signal Transduction Yeasts |
| Ano: | 2010 |
| País: | Portugal |
| Tipo de documento: | outro |
| Tipo de acesso: | acesso aberto |
| Instituição associada: | Universidade do Minho |
| Idioma: | inglês |
| Origem: | RepositóriUM - Universidade do Minho |
| Resumo: | [Excerpt] Cellular plasticity enables profound changes in cell phenotypes governed by tightly orchestrated interplay among distinct functional classes of regulatory molecules. This process typically involves the control of specific gene expression programs with distinct functional impacts on cellular behavior. One such manifestation of remarkable cellular plasticity— epithelial-mesenchymal transition (EMT)—has recently attracted broad interest in the field of cancer research, nearly 30 years after the pioneering work by Elizabeth Hay.1 EMT is a cell phenotype conversion utilized in tissue remodeling during embryonic development, re-enacted in adult tissue homeostasis (e.g. during regeneration upon injury) and in pathological conditions such as development of invasive and metastatic carcinomas or in fibrotic processes affecting vital organs such as the kidney or lungs.2,3 Cancer EMT has been recently demonstrated to generate breast carcinoma cancer stem-cells (CSCs) characterized by mesenchymal markers and by the capacity of self-renewal and of initiating secondary tumorigenesis.4 In addition, the process of EMT involves regulatory molecules (e.g., transcription factors Snail, Slug) that confer resistance to therapeutic induction of cell death. [...] |
|---|