Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2137201 | Leukemia Research | 2013 | 8 Pages |
Abstract
c-Myc has been implicated in a variety of hematologic malignancies including Burkitt's lymphoma. Targeting c-Myc driven growth pathways could be therapeutically useful but might require the identification of critical downstream proteins. Here we show that the serine–threonine kinase PBK/TOPK is frequently overexpressed in high-grade lymphomas and its expression is positively correlated to that of c-Myc and E2F1. Further we demonstrate that c-Myc regulates PBK expression through E2F1. Additionally, inhibition of c-Myc, E2F1 or PBK comparably decreased cell growth and survival. In conclusion, a c-Myc–E2F1–PBK signaling pathway operates in high-grade lymphomas and may provide a useful target for novel antineoplastic therapeutics.
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Authors
Fang Hu, Ronald B. Gartenhaus, Xianfeng F. Zhao, Hong-Bin Fang, Samuel Minkove, Daniella E. Poss, Aaron P. Rapoport,