title: Forced expression of YL-1 protein suppresses the anchorage-independent growth of Kirsten sarcoma virus-transformed NIH3T3 cells.
abstract: The YL-1 gene, encoding a novel nuclear protein with transcription factor-like features, has been isolated from the human chromosome 1q21, one of the regions supposedly carrying a transformation suppressor gene(s) for Kirsten sarcoma virus-transformed NIH3T3 (DT) cells. To test the suppressive activity of the YL-1 gene product, we forced the expression of human YL-1 cDNA in DT cells. The anchorage-independent growth (colony-forming ability in soft agar medium) was markedly suppressed in cells highly expressing the exogenous human YL-1 protein. Moreover, the soft agar clones, which were rarely originated from these cells, expressed reduced levels of exogenous YL-1 or none, with or without the loss/rearrangement of the introduced cDNA. In control experiments, cells carrying an introduced vector alone or an antisense-strand expression plasmid grew in soft agar as efficiently as parental DT cells. In contrast to the suppression of anchorage-independent growth, the forced expression of YL-1 did not effect the transformed phenotypes in adherent culture and tumorigenicity in nude mice. These findings not only indicated that the YL-1 protein functions as a transformation suppressor, but also suggest that it may be important for elucidating anchorage independence under separate genetic control from other transformed phenotypes.
authors.affiliation: Department of Molecular and Cell Genetics, School of Life Sciences, Faculty of Medicine, Tottori University, Yonago, Japan.
authors.forename: I
authors.initials: I
authors.lastname: Horikawa
authors.forename: H
authors.initials: H
authors.lastname: Tanaka
authors.forename: Y
authors.initials: Y
authors.lastname: Yuasa
authors.forename: M
authors.initials: M
authors.lastname: Suzuki
authors.forename: M
authors.initials: M
authors.lastname: Shimizu
authors.forename: M
authors.initials: M
authors.lastname: Oshimura
mesh_terms: D016475:3T3 Cells; D000818:Animals; D015152:Blotting, Northern; D015139:Blotting, Southern; D015153:Blotting, Western; D002448:Cell Adhesion / Q000235:genetics; D002471:Cell Transformation, Neoplastic / Q000235:genetics*; D002472:Cell Transformation, Viral / Q000235:genetics*; D004268:DNA-Binding Proteins / Q000096:biosynthesis* / Q000235:genetics; D006801:Humans; D007150:Immunohistochemistry; D007708:Kirsten murine sarcoma virus / Q000235:genetics*; D051379:Mice; D010957:Plasmids / Q000235:genetics; D012097:Repressor Proteins; D013489:Suppression, Genetic; D014157:Transcription Factors / Q000096:biosynthesis* / Q000235:genetics
chemical_list: D004268:DNA-Binding Proteins; D012097:Repressor Proteins; D014157:Transcription Factors; C092773:VPS72 protein, human; C484291:Vps72 protein, mouse