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.
Department of Molecular Genetics and Virology, Weizmann Institute of Science, Rehovot, Israel.
U
U
Glück
D J
DJ
Kwiatkowski
A
A
Ben-Ze'ev
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