title: Differentiation induction in the human rhabdomyosarcoma cell line TE-671. A morphological, biochemical and molecular analysis.
abstract: In the clonal human rhabdomyosarcoma cell line TE-671-1A, the expression of genes implicated in myogenic differentiation was determined before and after exposure to the differentiation inducers retinoic acid (RA), sodium butyrate (NaBut) and N-monomethylformamide (NMF). Exposure to NaBut or RA resulted in a significant (NaBut: p < 0.0001; RA: p < 0.05) increase in biochemical differentiation paralleled by a significant (NaBut: p < 0.0001; RA: p < 0.0002) inhibition of proliferation. An increase in the relative number of myotube-like giant cells was observed after exposure to NaBut. Exposure to NMF proved to be least effective and produced a significant (p < 0.0001) inhibition of proliferation without increase in differentiation. On the molecular level, exposure to RA resulted in a moderate increase in RAR a mRNA expression, whereas CRABP mRNA remained constant. RAR beta and RAR gamma mRNA were not expressed. mRNA expression of c-raf, c-myc and c-Ki-ras remained constant before and after exposure to all inducers of differentiation. C-fos mRNA was not expressed. In summary, differentiation can successfully be induced in the human rhabdomyosarcoma cell line TE-671-1A by various inducers of differentiation. In contrast to other myogenic cell lines, however, the proto-oncogenes myc, fos and raf are not involved in the transmission of myogenic differentiation signals in TE-671-1A cells.
authors.affiliation: Institute of Pathology, Düsseldorf, Germany.
authors.forename: U
authors.initials: U
authors.lastname: Ramp
authors.forename: C D
authors.initials: CD
authors.lastname: Gerharz
authors.forename: R
authors.initials: R
authors.lastname: Engers
authors.forename: N
authors.initials: N
authors.lastname: Marx
authors.forename: H E
authors.initials: HE
authors.lastname: Gabbert
mesh_terms: D000970:Antineoplastic Agents / Q000494:pharmacology*; D002087:Butyrates / Q000494:pharmacology*; D020148:Butyric Acid; D002454:Cell Differentiation / Q000187:drug effects / Q000502:physiology*; D002455:Cell Division / Q000187:drug effects; D002459:Cell Fusion / Q000187:drug effects; D002999:Clone Cells; D003402:Creatine Kinase / Q000378:metabolism; D005559:Formamides / Q000494:pharmacology*; D015870:Gene Expression / Q000187:drug effects; D006801:Humans; D007700:Kinetics; D008285:Major Histocompatibility Complex / Q000187:drug effects; D008854:Microscopy, Electron; D011519:Proto-Oncogenes / Q000187:drug effects; D012333:RNA, Messenger / Q000032:analysis / Q000096:biosynthesis; D018168:Receptors, Retinoic Acid / Q000096:biosynthesis; D012208:Rhabdomyosarcoma / Q000473:pathology* / Q000503:physiopathology / Q000648:ultrastructure; D013997:Time Factors; D014212:Tretinoin / Q000494:pharmacology*; D014407:Tumor Cells, Cultured
chemical_list: D000970:Antineoplastic Agents; D002087:Butyrates; D005559:Formamides; D012333:RNA, Messenger; D018168:Receptors, Retinoic Acid; D020148:Butyric Acid; D014212:Tretinoin; D003402:Creatine Kinase; C002950:methylformamide