Cargando…
Inflammation contributes to NKX3.1 loss and augments DNA damage but does not alter the DNA damage response via increased SIRT1 expression
The oxidative stress response is a cellular defense mechanism that protects cells from oxidative damage and cancer development. The exact molecular mechanism by which reactive oxygen species (ROS) contribute to DNA damage and increase genome instability in prostate cancer merits further investigatio...
Autores principales: | Debelec-Butuner, Bilge, Ertunc, Nursah, Korkmaz, Kemal Sami |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2015
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4336697/ https://www.ncbi.nlm.nih.gov/pubmed/25705129 http://dx.doi.org/10.1186/s12950-015-0057-4 |
Ejemplares similares
-
TNFα-Mediated Loss of β-Catenin/E-Cadherin Association and Subsequent Increase in Cell Migration Is Partially Restored by NKX3.1 Expression in Prostate Cells
por: Debelec-Butuner, Bilge, et al.
Publicado: (2014) -
NKX3.1 Expression
Contributes to Epithelial–Mesenchymal
Transition of Prostate Cancer Cells
por: Saydullaeva, Iroda, et al.
Publicado: (2023) -
The redox biology network in cancer pathophysiology and therapeutics
por: Manda, Gina, et al.
Publicado: (2015) -
Nkx3.1 controls the DNA repair response in the mouse prostate
por: Zhang, Hailan, et al.
Publicado: (2015) -
Loss of SIRT1 in diabetes accelerates DNA damage-induced vascular calcification
por: Bartoli-Leonard, Francesca, et al.
Publicado: (2020)