Kalebic T, Judde J G, Velez-Yanguas M, Knutsen T, Helman L J
Molecular Oncology Section, National Cancer Institute, Rockville Pike, Bethesda, Md 20892, USA.
Invasion Metastasis. 1996;16(2):83-96.
A new human metastatic rhabdomyosarcoma (RMS) model was established and analyzed for a number of biologic, cytogenetic and molecular parameters. Consistent with previous studies, the metastatic capacity of different RMS cell variants did not correlate with their tumorigenic or proliferative capacities. Interestingly, a highly metastatic variant was diploid, while a nonmetastatic variant was tetraploid, which parallels previous clinical observations. Genes whose expression had been found to be associated with either low- or high-metastatic capacity in carcinoma or melanoma did not show a similar association with different metastatic variants of RMS, derived from a mesenchymal tumor. We also found, in transient reporter gene assays, that several promoters had higher transcriptional activity in highly metastatic than in nonmetastatic RMS cell variants. This novel human RMS metastatic model may be instrumental for a better understanding of the regulatory pathways that control the metastatic phenotype of tumors of mesenchymal origin.
建立了一种新的人转移性横纹肌肉瘤（RMS）模型，并对其一些生物学、细胞遗传学和分子参数进行了分析。与先前的研究一致，不同RMS细胞变体的转移能力与其致瘤或增殖能力无关。有趣的是，高转移性变体是二倍体，而非转移性变体是四倍体，这与先前的临床观察结果相似。在癌或黑色素瘤中，其表达已被发现与低转移或高转移能力相关的基因，在源自间充质肿瘤的RMS不同转移变体中并未显示出类似的关联。我们还发现，在瞬时报告基因测定中，几个启动子在高转移性RMS细胞变体中的转录活性高于非转移性变体。这种新型的人RMS转移模型可能有助于更好地理解控制间充质起源肿瘤转移表型的调控途径。
