Peláez-Cristóbal, R. (Rafael)

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    The mammalian peptide adrenomedullin acts as a growth factor in tobacco plants
    (2017) Martinez, J.A. (José Alfredo); Niculcea, M. (Maria); Peláez-Cristóbal, R. (Rafael)
    Growth factors are extracellular signals that regulate cell proliferation and total body mass. Some animal growth factors can work on plant tissues and vice versa. Here we show that the mammalian growth factor adrenomedullin (AM) induces growth in tobacco plants. Addition of synthetic AM resulted in a dose-dependent growth of tobacco calluses. Furthermore, AM transgenic plants showed enhanced survival and significant increases in stem diameter, plant height, leaf length, weight of all organs, and a reduction in the time to flowering when compared to plants transformed with the control vector. These differences were maintained when organs were dried, resulting in a mean total biomass increase of 21.3%. The levels of soluble sugars and proteins in the leaves were unchanged between genotypes. AM transgenic plants had a significantly higher expression of cyclin D3 and the transcription factor E2FB than controls, suggesting that cell cycle regulation may be part of the intracellular signaling of AM in plants. In summary, mammalian AM increases vascular plants' survival and biomass with no apparent detriment of plant's morphological and/or biochemical properties, thus this strategy could be useful for crop productivity improvement.
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    β3 integrin expression is required for invadopodia-mediated ECM degradation in lung carcinoma cells
    (PLoS ONE, 2017) Larrayoz, I.M. (Ignacio M.); Rouzaut, A. (Ana); Ortiz-de-Solorzano, C. (Carlos); Garasa, S. (Saray); Peláez-Cristóbal, R. (Rafael); Morales-Urteaga, X. (Xabier); Salvo, E. (Elizabeth); Martinez, A. (Alfredo)
    Cancer related deaths are primarily due to tumor metastasis. To facilitate their dissemination to distant sites, cancer cells develop invadopodia, actin-rich protrusions capable of degrading the surrounding extracellular matrix (ECM). We aimed to determine whether β3 integrin participates in invadopodia formed by lung carcinoma cells, based on our previous findings of specific TGF-β induction of β3 integrin dependent metastasis in animal models of lung carcinoma. In this study, we demonstrate that lung carcinoma cells form invadopodia in response to TGF-β exposure. Invadopodia formation and degradation activity is dependent on β3 integrin expression since β3 integrin deficient cells are not able to degrade gelatin-coated surfaces. Even more, transient over-expression of SRC did not restore invadopodia formation in β3 integrin deficient cells. Finally, we observed that blockade of PLC-dependent signaling leads to more intense labeling for β3 integrin in invadopodia. Our results suggest that β3 integrin function, and location, in lung cancer cells are essential for invadopodia formation, and this integrin regulates the activation of different signal pathways necessary for the invasive structure. β3 integrin has been associated with poor prognosis and increased metastasis in several carcinoma types, including lung cancer. Our findings provide new evidence to support the use of targeted therapies against this integrin to combat the onset of metastases.