Regulation of cell death signaling by sorafenib in hepatocellular carcinoma. role of p53 gene family members

2013 ◽  
Vol 65 ◽  
pp. S39
Author(s):  
A.J. De la Rosa ◽  
A. Lovas ◽  
M. Müller ◽  
F.J. Padillo ◽  
J. Muntané
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Death ◽  
Gene Family ◽  
Family Members ◽  
P53 Gene ◽  
Cell Death Signaling

p53 family members – important messengers in cell death signaling in photodynamic therapy of cancer?

2015 ◽  
Vol 14 (8) ◽  
pp. 1390-1396 ◽  
Author(s):  
Pilar Acedo ◽  
Joanna Zawacka-Pankau
Keyword(s):  
Cell Death ◽  
Photodynamic Therapy ◽  
Tumor Suppressor ◽  
Cancer Cells ◽  
Cellular Stress ◽  
Family Members ◽  
P53 Family ◽  
Photodynamic Therapy Of Cancer ◽  
Cell Death Signaling

p53 is a powerful tumor suppressor and a critical sensor of cellular stress. This Perspective summarizes the role of p53 in response of cancer cells to photodynamic therapy – a field not fully explored yet.

Arsenic Trioxide-Induced Cell Death Occurs Partially Independent of the Pro-Apoptotic Bcl-2-Family Members Bax and Bak.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 4585-4585
Author(s):  
Christian Scholz ◽  
Antje Richter ◽  
Anja Richter ◽  
Bernd Dörken ◽  
Peter T. Daniel
Keyword(s):  
Cell Death ◽  
Arsenic Trioxide ◽  
Cell Lines ◽  
Apoptotic Cell ◽  
Family Members ◽  
Death Receptor ◽  
Hematologic Malignancies ◽  
Mitochondrial Pathway ◽  
Cell Death Pathways

Abstract Arsenic trioxide (As2O3, arsenite) efficiently kills cells from various hematologic malignancies and has successfully been employed for the treatment of acute promyelocytic leukaemia, myelodysplastic syndrome, and multiple myeloma. Investigating the mechanisms of arsenic trioxide-induced cell death, we recently demonstrated that arsenite-mediated cell demise has a partially necrotic phenotype, occurs independently of the extrinsic death receptor pathway of apoptosis, and is not hampered by the absence of functioning caspases. On the contrary, cell death proceeded entirely via an intrinsic, mitochondrial pathway and was efficiently blocked by the anti-apoptotic Bcl-2 family members Bcl-2 or Bcl-xL. Here, we address the role of the pro-apoptotic multi-domain Bcl-2 family members Bax and Bak. By employing different cell lines deficient for Bax and/or Bak, we demonstrate that Bax- or Bak-deficiency as well as the combined absence only partially blocks arsenite-induced cell death. While the detection of an additive effect of the combined Bax-/Bak-deficiency argues for a non redundant function of Bax and Bak, the persistence of a substantial percentage of arsenite-mediated cell demise in different double deficient cell lines nevertheless suggests a mode of arsenic trioxide-mediated cell death independent from these central inducers of apoptotic cell demise. The presented data add to the notion that arsenic trioxide kills tumor cells independent of the apoptotic machinery, and warrants further investigation on the efficacy of this compound in malignancies with deficiencies of the apoptotic cell death pathways.

scholarly journals The Three Clades of the Telomere-AssociatedTLOGene Family of Candida albicans Have Different Splicing, Localization, and Expression Features

2012 ◽  
Vol 11 (10) ◽  
pp. 1268-1275 ◽  
Author(s):  
Matthew Z. Anderson ◽  
Joshua A. Baller ◽  
Keely Dulmage ◽  
Lauren Wigen ◽  
Judith Berman
Keyword(s):  
Candida Albicans ◽  
Gene Family ◽  
Transcription Regulation ◽  
Family Members ◽  
Gene Products ◽  
Content Type ◽  
Human Host ◽  
Wide Range ◽  
N Terminus

ABSTRACTCandida albicansgrows within a wide range of host niches, and this adaptability enhances its success as a commensal and as a pathogen. The telomere-associatedTLOgene family underwent a recent expansion from one or two copies in other CUG clade members to 14 expressed copies inC. albicans. This correlates with increased virulence and clinical prevalence relative to those of otherCandidaclade species. The 14 expressedTLOgene family members have a conserved Med2 domain at the N terminus, suggesting a role in general transcription. The C-terminal half is more divergent, distinguishing three clades: clade α and clade β have no introns and encode proteins that localize primarily to the nucleus; clade γ sometimes undergoes splicing, and the gene products localize within the mitochondria as well as the nuclei. Additionally,TLOα genes are generally expressed at much higher levels than areTLOγ genes. We propose that expansion of theTLOgene family and the predicted role of Tlo proteins in transcription regulation provideC. albicanswith the ability to adapt rapidly to the broad range of different environmental niches within the human host.

scholarly journals Role of p63 and p73 isoforms on the cell death in patients with hepatocellular carcinoma submitted to orthotopic liver transplantation

PLoS ONE ◽  
2017 ◽  
Vol 12 (3) ◽  
pp. e0174326 ◽  
Author(s):  
Raúl González ◽  
Ángel J. De la Rosa ◽  
Alessandro Rufini ◽  
María A. Rodríguez-Hernández ◽  
Elena Navarro-Villarán ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Transplantation ◽  
Cell Death ◽  
Orthotopic Liver Transplantation

scholarly journals The Role of IL-1 Family Members and Kupffer Cells in Liver Regeneration

2016 ◽  
Vol 2016 ◽  
pp. 1-6 ◽  
Author(s):  
Quanhui Tan ◽  
Jianjun Hu ◽  
Xiaolan Yu ◽  
Wen Guan ◽  
Huili Lu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Regeneration ◽  
Receptor Antagonist ◽  
Kupffer Cells ◽  
Liver Diseases ◽  
Close Association ◽  
Interleukin 1 ◽  
Family Members ◽  
Systemic Review

Interleukin-1 (IL-1) family and Kupffer cells are linked with liver regeneration, but their precise roles remain unclear. IL-1 family members are pleiotropic factors with a range of biological roles in liver diseases, inducing hepatitis, cirrhosis, and hepatocellular carcinoma, as well as liver regeneration. Kupffer cells are the main source of IL-1 and IL-1 receptor antagonist (IL-1Ra), the key members of IL-1 family. This systemic review highlights a close association of IL-1 family members and Kupffer cells with liver regeneration, although their specific roles are inconclusive. Moreover, IL-1 members are proposed to induce effects on liver regeneration through Kupffer cells.

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