Inhibition of PAX2 expression results in alternate cell death pathways in prostate cancer cells differing in p53 status.
Inhibition of apoptosis is a critical pathophysiological factor that contributes to the development of prostate cancer. Recently, PAX2, a transcriptional regulator implicated in oncogenesis, has been demonstrated to be expressed by prostate cancer. However, its downstream molecular pathways for suppression of apoptosis, other than the tumor suppressor gene p53, have yet to be elucidated. Here, we examine the effects of inhibiting PAX2 expression by prostate cancer cells that differ in p53 gene status. These data collectively demonstrate that PAX2 inhibition results in cell death independent of p53, and that additional tumor suppressors or cell death pathways may be inhibited by PAX2 in prostate cancer cells.
Gibson
Willietta
W
Department of Pathology and Laboratory Medicine, Medical University of South Carolina, Suite 309, Charleston, SC 29425, USA.
Green
Ashley
A
Bullard
Rebecca S
RS
Eaddy
Andre C
AC
Donald
Carlton D
CD
D015153:Blotting, Western; D020169:Caspases / Q000378:metabolism; D016923:Cell Death / Q000502:physiology*; D045744:Cell Line, Tumor; D006801:Humans; D008297:Male; D018613:Microscopy, Confocal; D051762:PAX2 Transcription Factor / Q000037:antagonists & inhibitors / Q000096:biosynthesis*; D011471:Prostatic Neoplasms / Q000235:genetics / Q000378:metabolism*; D034741:RNA, Small Interfering; D020133:Reverse Transcriptase Polymerase Chain Reaction; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism*
D051762:PAX2 Transcription Factor; C497318:PAX2 protein, human; D034741:RNA, Small Interfering; D016159:Tumor Suppressor Protein p53; D020169:Caspases