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Journal of Biochemistry Advance Access published online on February 16, 2007
Journal of Biochemistry, doi:10.1093/jb/mvm059
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© 2007 The Japanese Biochemical Society

JB Review

Regulation of cellular transformation by oncogenic and normal Abl kinases

Jun Suzuki1,2 and Tomoyuki Shishido1,*

1Laboratory of Molecular Oncology, Nara Institute of Science and Technology, 8916-5 Takayama, Ikoma, Nara, 630-0192
2Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka, 565-0871

*To whom correspondence should be addressed. Tel: +81-743-72-5541, Fax: +81-743-72-5549; E-mail: shishid{at}bs.naist.jp

Received September 1, 2006; Accepted February 9, 2007


  Abstract

Cellular transformation, the conversion of normal cells into tumorigenic cells in vitro, is characterized by immortalization, anchorage- and serum-independent growth, and tumor formation in the nude mouse. Among these, anchorage-independent growth is one of the defining characteristics of transformed cells and tumor cells. Without attachment to the extracellular substrate, most normal cells cannot grow or survive, but tumor cells can proliferate. Many oncogenes and tumor suppressors are involved in regulating this process, among which is Abl tyrosine kinases. Previous work showed that v-Abl, an oncogenic variant of c-Abl kinase, induces anchorage-independent growth in the context of p53 deficiency, and a recent study by our group showed that loss of c-Abl kinase also facilitates anchorage-independent growth. The cellular context, such as a deficiency in both p53 and RB, is critical to induce anchorage independence by loss of c-Abl kinase. In this review, we discuss the mechanisms of cellular transformation by oncogenic and normal Abl kinases.

Key Words: cellular transformation, anchorage independence, Abl kinases, c-Abl, Bcr-Abl, v-Abl


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