Expression of members of the myf gene family in human rhabdomyosarcomas

Abstract

Summary Northern analysis of tumour RNA has been used to examine the expression of members of the myf family of muscle determining genes (myf3, myf4, myf5 and (Davies et al., 1987) and the rat myogenin gene (Wright et al., 1989) which were both isolated by procedures involving subtractive cDNA hybridisation. Subsequently Braun et al. (1989b, 1990) isolated two related genes designated myf5 and myf6 from a human foetal muscle cDNA library and an additional two genes called myf3 and myf4 (Braun et al., 1989a) that are the human homologues of, respectively, MyoDI and myogenin.

cDNA microarrays detect activation of a myogenic transcription program by the PAX3-FKHR fusion oncogene

“…HSIX1 was expressed at high levels in all five ARMS and in A204 and, in accord with published reports (22), at low levels in normal muscle. As expected, expression of MYOG (23) and IGF2 (24) was high in all five ARMS but not A204. The expression of IGFBP5, not previously described in ARMS, evident in all five of the cell lines, was particularly high in RH5.…”

“…We observed the remarkable ability of PAX3-FKHR to induce a myogenic transcription program, which includes induction of two important myogenic basic helix-loop-helix factors, Myogenin and MyoD, which are also expressed in ARMS (23). In addition, we observed induction of genes that represent several other key aspects of muscle function, including growth, energy metabolism, and contractility ( Table 1).…”

Regulation of acetylcholine receptor gene expression in human myasthenia gravis muscles. Evidences for a compensatory mechanism triggered by receptor loss.

“…5), a 1.8-Kb myogenin transcript and a 1.5-Kb MRF4 transcript were detected in all muscle samples, whereas MyoD1 and Myf5 transcripts were not detected in any of the samples tested (data not shown). The rabdomyosarcoma TE671 cell line, used as control, contained only the 1.8-Kb myogenin transcript, suggesting differential expression of myogenic factor genes in human muscle and rabdomyosarcomas (46). A semi-quantitative analysis was then performed by using densitometry with the 18S oligonucleotide probe as a control for the total amount of RNA loaded on the filter.…”

Tumor Cell Complementation Groups Based on Myogenic Potential: Evidence for Inactivation of Loci Required for Basic Helix-Loop-Helix Protein Activity

“…Gels were capillary transferred to Hybond-N and UV cross-linked. Blots were hybridized with probes for myosin light chain (MLC) (hA5- 13 Immunohistochemistry test and 5-bromo-4-chloro-3-indolyl-␤-D-galactopyranoside (X-Gal) staining. Cells were washed once in phosphate-buffered saline (PBS), fixed in 2% paraformaldehyde for 7 min, washed twice in PBS, and permeabilized in 0.25% Triton for 10 min.…”

“…Loss-of-function mutations analogous to those characterized in the general cell cycle machinery have not been widely identified, although a limited number of cell fusion experiments suggest that some tumor-derived cell lines contain loss-of-function alterations preventing terminal differentiation (4). An example of this is provided by cell lines derived from rhabdomyosarcomas, which express members of the MyoD family of basic helix-loop-helix (bHLH) proteins (13). The MyoD family orchestrates skeletal myogenesis (for reviews, see references 45 and 65), and a subset of rhabdomyosarcomas fails to differentiate into skeletal muscle because of the loss of a factor required for MyoD family activity (62).…”