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J. Biol. Chem., Vol. 278, Issue 51, 50915-50922, December 19, 2003

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Increased Expression of Bcl-xL and c-Myc Is Associated with Transformation by Abelson Murine Leukemia Virus^*

E. Jacintha Noronha, Karen Hinrichs Sterling, and Kathryn L. Calame¶

From the Departments ofMicrobiology and Biochemistry and Molecular Biophysics, Columbia University College of Physicians and Surgeons, New York, New York 10032

Transformation mediated by the v-Abl oncoprotein, a tyrosine kinase encoded by the Abelson murine leukemia virus, is a multi-step process requiring genetic alterations in addition to expression of v-Abl. Loss of p53 or p19ARF was previously shown to be required for Abelson murine leukemia virus transformation of primary mouse embryonic fibroblasts (MEFs). By comparing gene expression patterns in primary p53^-/- MEFs acutely infected with the v-Abl retrovirus, v-Abl-transformed MEF clones, and v-Abl-transformed MEF clones treated with Abl kinase inhibitor STI 571, we have identified additional genetic alterations associated with v-Abl transformation. Bcl-xL mRNA was elevated in three of five v-Abl-transformed MEF clones. In addition, elevated expression of c-Myc mRNA, caused either by c-myc gene amplification or by enhanced signaling via STAT3, was observed in five v-Abl-transformed MEF clones. The data suggest that increases in cell survival associated with Bcl-xL and increases in cell growth associated with c-Myc facilitate the transformation process dependent on constitutive mitogenic signaling by v-Abl.

Received for publication, June 23, 2003 , and in revised form, September 29, 2003.

^* The costs of publication of this article were defrayed in part by the payment of page charges. This 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.: 212-305-3504; Fax: 212-305-1468; E-mail: klc1{at}columbia.edu.

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