Anti-CK-MM monoclonal antibody, clone A027-17186

A human tumor cell line designated RMS-GR was established from an embryonal rhabdomyosarcoma, The monolayer cells were polygonal, round or spindle-shaped, The RMS-GR cell line became stable with a doubling time of 42 h, Tumorigenicity of the cells was confirmed by heterotransplantion into nude mice. Electron microscopic images showed typical cytoplasmic inclusion of aggregated intermediate filaments and myofibril-like thin filaments. The expression of desmin, vimentin, actin and human myoglobin was recognized by cytofluorometric analyses, and a large fraction of CK-MM and small fractions of CK-BB and MCK-1 isoenzymes were found. Chromosomal analysis showed that the modal chromosome number was consistently near triploid with structural abnormalities mostly involving chromosomes 1, 3 and 8, and additional unidentified markers. No alteration of chromosome 2 was observed. The RMS-GR cell line may provide a system to identify genes which are involved in the pathogenic mechanism of rhabdomyosarcomas, and to investigate the modulation of myogenic differentiation.

HMG-CoA reductase inhibitors have been associated with skeletal muscle myopathy, ranging from asymptomatic elevations of serum creatine kinase (CK) activity to rhabdomyolysis. In this study, we assessed the effects of addition of different concentrations of simvastatin and pravastatin on growth and differentiation of cultured primary rat skeletal muscle cells. Protein concentration, CK activity and percentage CK-MM, which is a parameter for maturation, were determined. Effects were generally stronger if inhibitors were added to both growth and differentiation medium rather than only to differentiation medium. Addition of 25 mu M pravastatin caused only a decrease of CK activity. Addition of 1-5 mu M simvastatin resulted in a decrease of protein concentration, CK activity and percentage CK-MM, whereas 25 mu M simvastatin resulted in cell death. Addition of mevalonic acid or cholesterol could not prevent the effects of 1 mu M simvastatin. In addition, 1 mu M simvastatin did not influence the cholesterol and phospholipid content of the cells. Superfusion of cultured cells with simvastatin concentrations of 10 mu M and higher caused a transient increase of the cytoplasmic calcium concentration followed by an apparent second rise and cell puncture. The results indicate that HMG-CoA reductase inhibitors may affect skeletal muscle cell regeneration in vivo by a direct toxic effect on growth and differentiation.