TY - JOUR
T1 - E2F1 induces tumor cell survival via nuclear factor-κB-dependent induction of EGR1 transcription in prostate cancer cells
AU - Zheng, Chaogu
AU - Ren, Zijia
AU - Wang, Hetian
AU - Zhang, Weici
AU - Kalvakolanu, Dhananjaya V.
AU - Tian, Zhigang
AU - Xiao, Weihua
PY - 2009/3/15
Y1 - 2009/3/15
N2 - Transcription factor E2F1 has been implicated in both apoptosis-promoting and apoptosis-suppressing effects. However, factors that mediate its antiapoptotic effects are still not identified. Using prostate tumor-derived cell lines, we showed here that E2F1 activated the expression of transcription factor EGR1 for promoting cell survival. E2F1 up-regulated the production of EGR1-induced growth factors, epidermal growth factor, platelet-derived growth factor, and insulin-like growth factor II, which in turn activated the phosphoinosi- tide-3-kinase/Akt pathway to resist drug-induced apoptosis. Moreover, E2F1 directly induced the transcription of the Egrl gene using the κB site located in its proximal promoter. E2F1 physically interacted with the RelA subunit of nuclear factor-κB and modulated its transactivity to fully activate EGR1 transcription. Together, these studies uncovered a novel mechanism for E2Fl-induced suppression of apoptosis in prostate cancer.
AB - Transcription factor E2F1 has been implicated in both apoptosis-promoting and apoptosis-suppressing effects. However, factors that mediate its antiapoptotic effects are still not identified. Using prostate tumor-derived cell lines, we showed here that E2F1 activated the expression of transcription factor EGR1 for promoting cell survival. E2F1 up-regulated the production of EGR1-induced growth factors, epidermal growth factor, platelet-derived growth factor, and insulin-like growth factor II, which in turn activated the phosphoinosi- tide-3-kinase/Akt pathway to resist drug-induced apoptosis. Moreover, E2F1 directly induced the transcription of the Egrl gene using the κB site located in its proximal promoter. E2F1 physically interacted with the RelA subunit of nuclear factor-κB and modulated its transactivity to fully activate EGR1 transcription. Together, these studies uncovered a novel mechanism for E2Fl-induced suppression of apoptosis in prostate cancer.
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U2 - 10.1158/0008-5472.CAN-08-4113
DO - 10.1158/0008-5472.CAN-08-4113
M3 - Article
C2 - 19276347
AN - SCOPUS:65549146911
VL - 69
SP - 2324
EP - 2331
JO - Journal of Cancer Research
JF - Journal of Cancer Research
SN - 0099-7013
IS - 6
ER -