Full metadata record
DC Field | Value | Language |
---|---|---|
dc.creator | Sanchez-Quiles, V. (Virginia) | - |
dc.creator | Santamaria, E. (Enrique) | - |
dc.creator | Segura, V. (Víctor) | - |
dc.creator | Sesma, L. (Laura) | - |
dc.creator | Prieto, J. (Jesús) | - |
dc.creator | Corrales, F.J. (Fernando José) | - |
dc.date.accessioned | 2012-04-03T11:28:15Z | - |
dc.date.available | 2012-04-03T11:28:15Z | - |
dc.date.issued | 2010 | - |
dc.identifier.citation | Sanchez-Quiles V, Santamaria E, Segura V, Sesma L, Prieto J, Corrales FJ. Prohibitin deficiency blocks proliferation and induces apoptosis in human hepatoma cells: molecular mechanisms and functional implications. Proteomics 2010 Apr;10(8):1609-1620. | es_ES |
dc.identifier.issn | 1615-9861 | - |
dc.identifier.uri | https://hdl.handle.net/10171/21553 | - |
dc.description.abstract | Prohibitin is a multifunctional protein participating in a plethora of essential cellular functions, such as cell signaling, apoptosis, survival and proliferation. In the liver, deficient prohibitin activity participates in the progression of non-alcoholic steatohepatitis and obesity, according to mechanisms that still must be elucidated. In this study, we have used a combination of transcriptomics and proteomics technologies to investigate the response of human hepatoma PLC/PRF/5 cells to prohibitin silencing to define in detail the biological function of hepatic Phb1 and to elucidate potential prohibitin-dependent mechanisms participating in the maintenance of the transformed phenotype. Abrogation of prohibitin reduced proliferation and induced apoptosis in human hepatoma cells in a mechanism dependent on NF kappaB signaling. Moreover, down-regulation of ERp29 together with down-regulation of Erlin 2 suggests ER stress. In agreement, increased C/EBP homologous protein levels, poly-ADP ribose polymerase cleavage and activation of caspase 12 and downstream caspase 7 evidenced ER stress-induced apoptosis. Down-regulation of proteasome activator complex subunit 2 and stathmin as well as accumulation of ubiquitinated proteins suggest interplay between ER stress and proteasome malfunction. Taken together, our results provide evidences for prohibitin having a central role in the maintenance of the transformed and invasive phenotype of human hepatoma cells and may further support previous studies suggesting prohibitin as a potential clinical target. | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | Wiley-VCH Verlag Berlin | es_ES |
dc.rights | info:eu-repo/semantics/closedAccess | - |
dc.subject | Apoptosis | es_ES |
dc.subject | Cell biology | es_ES |
dc.subject | Hepatoma | es_ES |
dc.subject | Prohibitin | es_ES |
dc.subject | Proliferation | es_ES |
dc.title | Prohibitin deficiency blocks proliferation and induces apoptosis in human hepatoma cells: molecular mechanisms and functional implications | es_ES |
dc.type | info:eu-repo/semantics/article | es_ES |
dc.relation.publisherversion | http://onlinelibrary.wiley.com/doi/10.1002/pmic.200900757/abstract | es_ES |
dc.type.driver | info:eu-repo/semantics/article | es_ES |
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