South Korean scientists found that adenylate kinase 2 (AK2) activates an apoptotic pathway that is absent in certain tumor cell lines.
The team discovered that AK2, through the formation of an AK2–FADD–caspase-10 (AFAC10) complex, mediates mitochondrial apoptosis. They also showed that downregulation of AK2 reduces etoposide- or staurosporine-induced apoptosis in human cells but does not decrease that induced by tumor-necrosis-factor-related apoptosis-inducing ligand (TRAIL) or Fas ligand (FasL).
The scientists also examined some etoposide-resistant human tumor cell lines but could not detect the AFAC10 complexes. “Taken together, these results suggest that acting in concert with FADD and caspase-10, AK2 mediates a novel intrinsic apoptotic pathway that may be involved in tumorigenesis,” according to the researchers.
The study was performed by investigators at the Gwangju Institute of Science and Technology, Seoul National University, Hanyang University, and Korea Institute of Science and Technology. The paper appears online in Nature Cell Biology.