Key result
PON2 overexpression drives chemotherapy resistance by lowering CHOP, while knock-down induces tumor cell apoptosis.
Why the study?
Oxidative damage and ER stress-induced apoptosis contribute to atherosclerosis and cancer treatment resistance, but the role of PON2 in tumorigenesis and apoptotic escape was unknown.
Does PON2 overexpression or knock-down alter apoptosis resistance and cell death in tumor cell models?
Population
Human tumor samples and cell culture models
Comparison
PON2 overexpression vs PON2 knock-down or control cells
Design
Preclinical experimental study
Authors
Loading...
PON2 may represent an anti-tumor target; hypothesis-generating and leaves open clinical translation.
Does PON2 overexpression or knock-down alter apoptosis resistance and cell death in tumor cell models?
PON2 overexpression in tumors provides resistance to apoptosis and chemotherapeutics, suggesting PON2 as a potential novel anti-tumor target.
Witte et al. (2011) studied Cancer (n=4,430). PON2 overexpression or knock-down vs. Naive cells or scrambled siRNA was evaluated on Apoptosis and cell death in response to chemotherapeutics or ER stress. PON2 overexpression provides resistance to chemotherapeutics by lowering redox-triggered induction of pro-apoptotic CHOP, whereas PON2 knock-down causes apoptosis of selective tumor cells.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: