Cell cycle and Oncology (CyCLOn )
The Cell cycle and Oncology Group was established in 2003. A major goal of the lab has been to study the cellular and molecular basis of cancer. For a decade, our effort was aimed to discover new cooperative functions of cell cycle regulators and to identify cell cycle independent roles of cdk-inhibitors. Our work has contributed to the identification of new functions of the cell cycle inhibitors in angiogenesis (Vidal et al PNAS 2005), endochondral bone formation (Yeh et al MCB 2007) or stem cell biology (Li et al Cell Stem Cell 2012; Porlan et al Nat Neurosci 2013; Vilas et al Oncotarget 2015).
In recent years, the group has been devoted to explore new therapeutic strategies in cancer by using nanomedicines (Borrajo et al J Control Rel 2016; Amaral et al Angew Chem 2018; Goldberg et al Nat Commun 2022), atomic quantum clusters (Porto et al Adv Funct Mater 2022) and immunotherapy (Retos Colaboración with SunRock Biopharma and two current grants for immunotherapy against ovarian cancer).
- Molecular mechanisms of oncogenesis: cell cycle and cancer.
- Search for new tumor markers and therapeutic targets.
- Validation of new therapeutic strategies in cancer.
- Development of refined animal models of advanced cancer.
Rho acivity can alter the translation of p27 mRNA and is important for RasV12 induced transformation in a manner dependent on p27 status.
p130 and p27 co-operate to control mobilization of angiogenic progenitors from the bone marrow.
Cooperation between p27 and p107 during endochondral ossification suggests a genetic pathway controlled by p27 and p130.
p27Kip1 directly contributes to Sox2 transcriptional repression during embryonic stem cell differentiation.
Transcriptional repression of Bmp2 by p21(Waf1/Cip1) links quiescence to neural stem cell maintenance
Transcriptional regulation of Sox2 by the retinoblastoma family of pocket proteins.
Context-Dependent Impact of RAS Oncogene Expression on Cellular Reprogramming to Pluripotency
Silver Clusters of Five Atoms as Highly Selective Antitumoral Agents Through Irreversible Oxidation of Thiols