Suppression of tumorigenicity in simian virus 40-transformed 3T3 cells transfected with alpha-actinin cDNA.
Human cytoskeletal alpha-actinin cDNA was transfected into highly malignant simian virus 40-transformed BALB/c 3T3 (SVT2) cells that express 6-fold lower levels of alpha-actinin than nontransformed BALB/c 3T3 cells. SVT2 clones expressing various levels of alpha-actinin were isolated and their structure and tumorigenic properties were determined. Transfected SVT2 clones expressing alpha-actinin at levels found in nontumorigenic 3T3 cells displayed a flatter phenotype, a decreased ability to grow in suspension culture in soft agar, and a marked reduction in their ability to form tumors in syngeneic BALB/c mice and in athymic nude mice. Clones overexpressing alpha-actinin at the highest level (about 2-fold higher than 3T3 cells) were completely suppressed in their ability to form tumors in syngeneic BALB/c mice. The results suggest that alpha-actinin, an actin-crosslinking protein that is also localized in cell junctions, may have an effective suppressive ability on the transformed phenotype.
Glück
U
U
Department of Molecular Genetics and Virology, Weizmann Institute of Science, Rehovot, Israel.
Kwiatkowski
D J
DJ
Ben-Ze'ev
A
A
D016475:3T3 Cells / Q000166:cytology; D000185:Actinin / Q000235:genetics* / Q000378:metabolism; D000818:Animals; D002472:Cell Transformation, Viral / Q000235:genetics*; D005455:Fluorescent Antibody Technique; D006801:Humans; D051379:Mice; D008807:Mice, Inbred BALB C; D008819:Mice, Nude; D009374:Neoplasms, Experimental / Q000209:etiology; D013539:Simian virus 40 / Q000235:genetics* / Q000472:pathogenicity; D014162:Transfection
D000185:Actinin