Ehrlich ascites tumor cells produce a transforming growth factor-β (TGFβ)-like activity but lack receptors with TGFβ-binding capacity

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Títol: Ehrlich ascites tumor cells produce a transforming growth factor-β (TGFβ)-like activity but lack receptors with TGFβ-binding capacity
Autors: Elexpuru Artetxe, Ana | Martín-Nieto, José | Jiménez Martínez, Amparo | Gómez Torres, Carmen | Villalobo Polo, Antonio
Grups d'investigació o GITE: Genética Humana y de Mamíferos
Centre, Departament o Servei: Universidad de Alicante. Departamento de Fisiología, Genética y Microbiología | Instituto de Investigaciones Biomédicas
Paraules clau: Transforming growth factor-β receptors | Ehrlich ascites tumor cells
Àrees de coneixement: Genética
Data de creació: 6-d’agost-1996
Data de publicació: de maig-1997
Editor: Kluwer Academic Publishers
Citació bibliogràfica: ELEXPURU ARTETXE, Ana, et al. "Ehrlich ascites tumor cells produce a transforming growth factor-β (TGFβ)-like activity but lack receptors with TGFβ-binding capacity". Molecular and Cellular Biochemistry. Vol. 170, No. 1-2 (May 1997). ISSN 0300-8177, pp. 153-162
Resum: Ehrlich ascites tumor cells incorporate [methyl-3H]thymidine into DNA independently of exogenous growth factors or fetal calf serum. Using an acid/ethanol extraction procedure we have obtained from these tumor cells a fraction that induces both the proliferation and the formation of cell foci by Swiss 3T3 mouse fibroblasts in the presence of insulin; inhibits the proliferation of Mv1Lu mink lung epithelial cells; and stimulates the growth of NRK rat kidney fibroblasts in soft-agar in the presence of epidermal growth factor. An antibody against transforming growth factor-β (TGFβ) prevents both the tumor extract-induced proliferation of Swiss 3T3 fibroblasts and the tumor extract-induced proliferative arrest of Mv1Lu cells. The tumor cells secrete a TGFβ-like activity to the extracellular medium in a partially-activated form. However, authentic TGFβ does not affect their proliferation, and no TGFβ receptors were detected using [125I]TGFβ as a ligand. Therefore, the absence of TGFβ receptors with ligand-binding capacity in these tumor cells may bypass the negative control that this factor exerts on the proliferation of their normal cell counterparts.
Patrocinadors: This work was supported by Grants to A.V. from the Comisión Interministerial de Ciencia y Tecnología (SAF392/93 and SAF96-35) and from the Dirección General de Investigación Científica y Técnica (PR94-343).
URI: http://hdl.handle.net/10045/9728
ISSN: 0300-8177 (Print) | 1573-4919 (Online)
DOI: 10.1023/A:1006809604193
Idioma: eng
Tipus: info:eu-repo/semantics/article
Drets: The original publication is available at www.springerlink.com
Revisió científica: si
Versió de l'editor: http://dx.doi.org/10.1023/A:1006809604193
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