Froeschlé A, Carnac G, Alric S, Montarras D, Pinset C, Rochette-Egly C, Bonnieu A
Laboratoire de Différenciation Cellulaire et Croissance, Institut National de la Recherche Agronomique, Montpellier, France.
Oncogene. 1996 Jan 18;12(2):411-21.
In C2 muscle cells, retinoic acid (RA) induces growth arrest associated with terminal differentiation. These RA actions are presumed to be mediated through nuclear receptors (RARs and RXRs) that belong to the superfamily of ligand-dependent transcription factors. In this study, we have characterized a myogenic C2 subclone, that unlike parental cells, is resistant to growth inhibition and differentiation by RA. Examination of these RA-sensitive and resistant C2 cells for the expression of retinoid acid receptors revealed a lack of RXR alpha expression at the myoblast stage in resistant C2 cells. To determine the functions of RXR alpha, we introduced an RXR alpha expression vector into RA-resistant C2 cells by transient or stable transfections. Our results show that RXR alpha restores the response to RA in this subclone with respect to AP1 inhibition and growth arrest. These observations indicate that RXR alpha plays a crucial role in mediating RA induced growth arrest of C2 myogenic cells.
在C2肌细胞中，视黄酸（RA）诱导与终末分化相关的生长停滞。这些RA作用被认为是通过属于配体依赖性转录因子超家族的核受体（RARs和RXRs）介导的。在本研究中，我们鉴定了一个成肌C2亚克隆，它与亲代细胞不同，对RA诱导的生长抑制和分化具有抗性。检测这些对RA敏感和抗性的C2细胞中类视黄酸受体的表达，发现抗性C2细胞在成肌细胞阶段缺乏RXRα表达。为了确定RXRα的功能，我们通过瞬时或稳定转染将RXRα表达载体导入对RA抗性的C2细胞中。我们的结果表明，RXRα在该亚克隆中恢复了对RA在抑制AP1和生长停滞方面的反应。这些观察结果表明，RXRα在介导RA诱导的C2成肌细胞生长停滞中起关键作用。
