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Originally published In Press as doi:10.1074/jbc.M111501200 on January 4, 2002

J. Biol. Chem., Vol. 277, Issue 10, 8076-8082, March 8, 2002
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Functional Cooperation among Ras, STAT5, and Phosphatidylinositol 3-Kinase Is Required for Full Oncogenic Activities of BCR/ABL in K562 Cells*

Junko SonoyamaDagger , Itaru MatsumuraDagger , Sachiko EzoeDagger , Yusuke SatohDagger , Xian ZhangDagger , Yoshihisa KataokaDagger , Emi TakaiDagger , Masao MizukiDagger , Takashi MachiiDagger , Hiroshi Wakao§, and Yuzuru KanakuraDagger

From the Dagger  Department of Hematology/Oncology, Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka 565-0871 and the § Helix Research Institute, 1532-3 Yana Kisarazu-shi, Chiba 292-0812, Japan

BCR/ABL tyrosine kinase generated from the chromosomal translocation t(9;22) causes chronic myelogenous leukemia and acute lymphoblastic leukemia. To examine the roles of BCR/ABL-activated individual signaling molecules and their cooperation in leukemogenesis, we inducibly expressed a dominant negative (DN) form of Ras, phosphatidylinositol 3-kinase, and STAT5 alone or in combination in p210 BCR/ABL-positive K562 cells. The inducibly expressed DN Ras (N17), STAT5 (694F), and DN phosphatidylinositol 3-kinase (Delta p85) inhibited the growth by 90, 55, and 40%, respectively. During the growth inhibition, the expression of cyclin D2 and cyclin D3 was suppressed by N17, 694F, or Delta p85; that of cyclin E by N17; and that of cyclin A by Delta p85. In addition, N17 induced apoptosis in a small proportion of K562, whereas 694F and Delta p85 were hardly effective. In contrast, coexpression of two DN mutants in any combinations induced severe apoptosis. During these cultures, the expression of Bcl-2 was suppressed by N17, 694F, or Delta p85, and that of Bcl-XL by N17. Furthermore, although K562 was resistant to interferon-alpha - and dexamethasone-induced apoptosis, disruption of one pathway by N17, 694F, or Delta p85 sensitized K562 to these reagents. These results suggested that cooperation among these molecules is required for full leukemogenic activities of BCR/ABL.

* This work was supported by grants from the Ministry of Education, Science and Culture of Japan; the Mochida Foundation; the Ichiro Kanehara Foundation; the Uehara Memorial Foundation; the Naito Foundation; and the Japan Medical Association.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

To whom correspondence should be addressed. Tel.: 81-6-6879-3871; Fax: 81-6-6879-3879; E-mail: matumura@bldon.med.osaka-u. ac.jp.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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