Person:
Lorente Pérez, María Del Mar

Profile Picture
First Name
María Del Mar
Last Name
Lorente Pérez
URI
https://hdl.handle.net/20.500.14352/76270
Affiliation
Universidad Complutense de Madrid
Faculty / Institute
Ciencias Químicas
Department
Bioquímica y Biología Molecular
Area
Bioquímica y Biología Molecular
Identifiers
UCM identifierORCIDScopus Author IDWeb of Science ResearcherIDDialnet ID

Filters

2007 - 200922010 - 20141
Reset filters

Settings

Author: Carracedo, Arkaitz × Subject: 577.1 ×

Search Results

Now showing 1 - 3 of 3
  • Thumbnail Image
    Item
    Targeting Cannabinoid Receptors in Brain Tumors
    (Cannabinoids and the brain, 2008) Velasco Díez, Guillermo; Carracedo, Arkaitz; Blázquez Ortiz, Cristina; Lorente Pérez, María Del Mar; Aguado Sánchez, Tania; Sánchez García, María Cristina; Galve Roperh, Ismael; Guzmán Pastor, Manuel; Köfalvi, Attila
    Cannabinoids, the active components of Cannabis sativa L., act in the body by mimicking endogenous substances — the endocannabinoids — that activate specific cell surface receptors. Cannabinoids exert various palliative effects in cancer patients. In addition, cannabinoids inhibit the growth of different types of tumor cells, including glioma cells, in laboratory animals. They do so by modulating key cell signaling pathways, mostly the endoplasmic reticulum stress response, thereby inducing antitumoral actions such as the apoptotic death of tumor cells and the inhibition of tumor angiogenesis. Of interest, cannabinoids seem to be selective antitumoral compounds as they kill glioma cells but not their nontransformed astroglial counterparts. On the basis of these preclinical findings, a pilot clinical study of Δ9-tetrahydrocannabinol (Δ9-THC) in patients with recurrent glioblastoma multiforme has been recently run. The fair safety profile of Δ9-THC, together with its possible growth-inhibiting action on tumor cells, may set the basis for future trials aimed at evaluating the potential antitumoral activity of cannabinoids.
  • Thumbnail Image
    Item
    Loss of Tribbles pseudokinase-3 promotes Akt-driven tumorigenesis via FOXO inactivation
    (Cell Death and Differentiation, 2014) Salazar Roa, María; Lorente Pérez, María Del Mar; Garcia-Taboada, Elena; Pérez Gómez, Eduardo; Davila, Davila; Zuñiga, Patricia; Flores Landeira, Juana María; Rodriguez, Antonio; Hegedus, Zoltán; Mosen-Ansorena, David; Aransay, Ana María; Hernandez-Tiedra, Sonia; Lopez-Valero, Israël; Quintanilla, Miguel; Sanchez, Cristina; Iovanna, Juan; Dusetti, Nelson; Guzmán Pastor, Manuel; Francis, Sheila; Carracedo, Arkaitz; Kiss-Toth, Endre; Velasco Díez, Guillermo
    Tribbles pseudokinase-3 (TRIB3) has been proposed to act as an inhibitor of AKT although the precise molecular basis of this activity and whether the loss of TRIB3 contributes to cancer initiation and progression remain to be clarified. In this study, by using a wide array of in vitro and in vivo approaches, including a Trib3 knockout mouse, we demonstrate that TRIB3 has a tumor- suppressing role. We also find that the mechanism by which TRIB3 loss enhances tumorigenesis relies on the dysregulation of the phosphorylation of AKT by the mTORC2 complex, which leads to an enhanced phosphorylation of AKT on Ser473 and the subsequent hyperphosphorylation and inactivation of the transcription factor FOXO3. These observations support the notion that loss of TRIB3 is associated with a more aggressive phenotype in various types of tumors by enhancing the activity of the mTORC2/AKT/FOXO axis
  • Thumbnail Image
    Item
    Cannabinoids and Gliomas
    (Molecular Neurobiology, 2007) Velasco Díez, Guillermo; Carracedo, Arkaitz; Blázquez Ortiz, Cristina; Lorente Pérez, María Del Mar; Aguado Sánchez, Tania; Haro, Amador; Sánchez García, María Cristina; Galve Roperh, Ismael; Guzmán Pastor, Manuel
    Cannabinoids, the active components of Cannabis sativa L., act in the body by mimicking endogenous substances—the endocannabinoids—that activate specific cell surface receptors. Cannabinoids exert various palliative effects in cancer patients. In addition, cannabinoids inhibit the growth of different types of tumor cells, including glioma cells, in laboratory animals. They do so by modulating key cell signaling pathways, mostly the endoplasmic reticulum stress response, thereby inducing antitumoral actions such as the apoptotic death of tumor cells and the inhibition of tumor angiogenesis. Of interest, cannabinoids seem to be selective antitumoral compounds, as they kill glioma cells, but not their non-transformed astroglial counterparts. On the basis of these preclinical findings, a pilot clinical study of Δ9-tetrahydrocannabinol (THC) in patients with recurrent glioblastoma multiforme has been recently run. The good safety profile of THC, together with its possible growth-inhibiting action on tumor cells, justifies the setting up of future trials aimed at evaluating the potential antitumoral activity of cannabinoids.