Caracterización de los mecanismos moleculares asociados a la funcionalidad de Beta-Catenina en líneas celulares de cáncer de mamá con expresión diferencial de HER2
Between 15-20% of all breast cancers overexpress human epidermal growth factor receptor type 2 (HER2). Although the overexpression of HER2 identifies those women who will respond to therapy with Trastuzumab, not all patients will benefit from such treatment. Approximately, 15% of them will suffer re...
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| Autores principales: | , , , , , |
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| Publicado: |
2019
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| Materias: | |
| Acceso en línea: | https://bdigital.uncu.edu.ar/fichas.php?idobjeto=14656 |
| Sumario: | Between 15-20% of all breast cancers overexpress human epidermal growth factor receptor type 2 (HER2). Although the overexpression of HER2 identifies those women who will respond to therapy with Trastuzumab, not all patients will benefit from such treatment. Approximately, 15% of them will suffer relapse of the disease after the therapy, indicating the development of resistance. Several lines of evidence suggest the existence of important links between HER2 and proteins involved in cell adhesion such as beta catenin in breast cancer. However, results describing a relationship between the distribution / localization of beta-catenin and HER2 as a function of breast cancer progression are not available. In a recent study in women with breast cancer, we have described a correlation between the location of beta-catenin in the cell membrane and the distribution of HER2, associated with good prognosis; This data is of great value because the patients were not treated with Trastuzumab and had a prolonged follow-up of the disease (15 years). It is necessary to encourage the study of the correlation between beta-catenin and HER2 and the intervention of other molecules that would be responsible for maintaining β-catenin in the cell membrane, stabilizing the adherent junctions and improving the prognosis of the disease. At this point, the protein tyrosine phosphatase (PTP) and kinase (PKD1) play and important role because regulate beta catenin location and distribution mantaining cell cell adhesion. The main objective of this project is to evaluate if PTP1B and PKD1 are able to maintain the β-catenin in the membrane of the cells that over-express HER2 and to elucidate the molecular mechanisms responsible for such situation. The discovery of new proteins and their localization that are linked to the HER2 pathway as in the case of the Wnt / beta-catenin and PTP1B/PKD1 pathways is very necessary to avoid a therapy that could generate resistance and unnecessary economic costs in cancer patients of breast HER2 positive. |
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