Schwering Ines, Bräuninger Andreas, Distler Verena, Jesdinsky Julia, Diehl Volker, Hansmann Martin-Leo, Rajewsky Klaus, Küppers Ralf
Institute for Genetics, University of Cologne, Cologne, Germany.
Mol Med. 2003 Mar-Apr;9(3-4):85-95.
The malignant cells of classical Hodgkin's lymphoma (cHL), Hodgkin and Reed-Sternberg (HRS) cells, appear to be derived from germinal center (GC) B cells in most cases of the disease. Apart from recent findings of constitutive activation of some transcription factors and autocrine stimulation by cytokine receptors, the mechanisms of malignant transformation in cHL still remain poorly understood. We performed a large scale gene expression study using serial analysis of gene expression (SAGE), comparing the cHL cell line L1236 and human GC B cells. Semiquantitative RT-PCR was used to confirm results from the SAGE and to analyze gene expression in 3 additional cHL cell lines. To investigate expression of some genes in cHL cases, we applied RT-PCR on microdissected HRS cells. In total, 464 genes showed a change in expression level of 5-fold or higher. For 12 genes (out of 177) identified as upregulated in L1236 cells, RT-PCR confirmed the SAGE results and also showed elevated expression in 3 other cHL cell lines. For 3 of the upregulated genes, expression by HRS cells in the tissue also was confirmed. Several of the differentially expressed genes may play a role in the pathogenesis of cHL because they represent potential oncogenes, such as rhoC, L-myc, and PTP4A, or transcription factors, such as ATF-5, ATBF1, and p21SNFT. The genes that showed significantly deregulated expression in HRS cells should be helpful not only for the identification of genes involved in the pathogenesis of cHL but also for discovering potential prognostic markers or therapeutic targets.
经典型霍奇金淋巴瘤(cHL)的恶性细胞,即霍奇金和里德-斯腾伯格(HRS)细胞,在该疾病的大多数病例中似乎来源于生发中心(GC)B细胞。除了近期关于某些转录因子的组成性激活以及细胞因子受体自分泌刺激的研究发现外,cHL中恶性转化的机制仍知之甚少。我们使用基因表达序列分析(SAGE)进行了一项大规模基因表达研究,比较了cHL细胞系L1236和人GC B细胞。采用半定量逆转录聚合酶链反应(RT-PCR)来确认SAGE的结果,并分析另外3种cHL细胞系中的基因表达。为了研究cHL病例中某些基因的表达情况,我们对显微切割的HRS细胞应用了RT-PCR。总共464个基因的表达水平变化了5倍或更高。对于在L1236细胞中被鉴定为上调的12个基因(共177个),RT-PCR证实了SAGE的结果,并且在其他3种cHL细胞系中也显示出表达升高。对于其中3个上调基因,还证实了组织中HRS细胞的表达。一些差异表达基因可能在cHL的发病机制中起作用,因为它们代表潜在的癌基因,如rhoC、L-myc和PTP4A,或转录因子,如ATF-5、ATBF1和p21SNFT。在HRS细胞中显示出明显表达失调的基因不仅有助于鉴定参与cHL发病机制的基因,还能用于发现潜在的预后标志物或治疗靶点。