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Vol. 14, Issue 2, 585-599, February 2003
Regulates Mitogenic Signaling through Transcriptional
Induction of Cyclin D1 via Tcf
and
*The Albert Einstein Cancer Center, Division of
Hormone-Dependent Tumor Biology, The Albert Einstein Comprehensive
Cancer Center, Department of Developmental and Molecular Biology,
Albert Einstein College of Medicine, Bronx, New York 10461;
The Wnt/Department of Oncology, Lombardi Cancer Center
and Department of Cell Biology, Georgetown University School of
Medicine, Washington, DC 20007; Department of
Molecular Cell Biology, The Weizmann Institute of Science, Rehovot
76100, Israel; §Department of Medicine, Memorial
Sloan-Kettering Cancer Center, New York, New York 10021; and
Division of Hematology-Oncology, Department of
Medicine, Simmons Cancer Center, University of Texas Southwestern
Medical Center, Dallas, Texas 75235
-catenin/Tcf and I
B/NF-B cascades are independent
pathways involved in cell cycle control, cellular differentiation, and
inflammation. Constitutive Wnt/-catenin signaling occurs in certain
cancers from mutation of components of the pathway and from activating
growth factor receptors, including RON and MET. The resulting
accumulation of cytoplasmic and nuclear -catenin interacts with the
Tcf/LEF transcription factors to induce target genes. The IB kinase
complex (IKK) that phosphorylates IB contains IKK
, IKK, and
IKK
. Here we show that the cyclin D1 gene functions as a point of convergence between the Wnt/-catenin and IB
pathways in mitogenic signaling. Mitogenic induction of
G1-S phase progression and cyclin D1 expression was PI3K
dependent, and cyclin D1
/ cells
showed reduced PI3K-dependent S-phase entry. PI3K-dependent induction
of cyclin D1 was blocked by inhibitors of PI3K/Akt/IB/IKK or
-catenin signaling. A single Tcf site in the cyclin D1 promoter was
required for induction by PI3K or IKK. In
IKK/ cells, mitogen-induced DNA
synthesis, and expression of Tcf-responsive genes was reduced.
Reintroduction of IKK restored normal mitogen induction of cyclin D1
through a Tcf site. In IKK/ cells,
-catenin phosphorylation was decreased and purified IKK was
sufficient for phosphorylation of -catenin through its N-terminus in
vitro. Because IKK but not IKK induced cyclin D1 expression through Tcf activity, these studies indicate that the relative levels
of IKK and IKK may alter their substrate and signaling specificities to regulate mitogen-induced DNA synthesis through distinct mechanisms.
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