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Cell and Tumor Biology |
Departments of Pathology and Microbiology and New York University Cancer Institute, New York University School of Medicine, New York, New York
Requests for reprints: David E. Levy, Departments of Pathology and Microbiology and New York University Cancer Institute, New York University School of Medicine, 550 First Avenue, New York, NY 10016. Phone: 212-263-8192; Fax: 212-263-8211; E-mail: del243{at}med.nyu.edu.
Signal transducer and activator of transcription 3 (STAT3) has been indirectly implicated in numerous fundamental cellular processes, including proliferation, survival, and differentiation. We provide genetic evidence from studies of STAT3-null cells that STAT3 is dispensable for normal growth of mouse fibroblasts in culture. STAT3 contributed to the full induction of some (typified by c-fos) but not all (typified by c-myc) immediate early gene expression, but STAT3-independent processes were sufficient to support full cell growth and survival. However, STAT3 was required to manifest a transformed state following expression of v-src, and STAT3-null cells were impaired for anchorage-independent growth as colonies in soft agar and as tumors in mice. The data suggest that STAT3 mediates the maintenance of focal adhesion kinase activity in the absence of cell adhesion by suppressing the action of an inhibitory phosphatase.
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