Department of Human and Animal Cell Lines, DSMZ--German Collection of Microorganisms and Cell Cultures, Inhoffenstr. 7B, 38124 Braunschweig, Germany.
Genes Chromosomes Cancer. 2011 Dec;50(12):996-1009. doi: 10.1002/gcc.20920. Epub 2011 Aug 30.
Hodgkin/Reed-Sternberg (HRS) cells represent the malignant fraction of infiltrated lymph nodes in Hodgkin lymphoma (HL). Although HRS cells display multiple chromosomal aberrations, few are recurrent and the targeted genes unknown. However, understanding the pathology of HL and developing rational therapies may well require identifying putative deregulated genes. Here, we analyzed the karyotype of the well-defined HL cell line L-1236 by spectral karyotyping and identified multiple abnormalities, therein, notably t(4;8)(q27;q24) which includes two breakpoint regions previously highlighted in HL. Target genes at 4q27 and 8q24 were shortlisted by high density genomic arrays and fluorescence in situ hybridization. Expression analysis of candidate target genes revealed conspicuous activation of phosphodiesterase PDE5A at 4q27 and inhibition of homeobox gene ZHX2 at 8q24. Treatment of L-1236 with PDE5A-inhibitor sildenafil or with siRNA directed against PDE5A and concomitant stimulation with cyclic guanosine monophosphate (cGMP) resulted in enhanced apoptosis, indicating PDE5A as an oncogene. Expression profiling of L-1236 cells following siRNA-mediated knockdown of ZHX2 showed inhibition of genes regulating differentiation and apoptosis, suggesting tumor suppressor activity of ZHX2. Downstream genes included STAT1 and several STAT1-target genes, indicating activation of STAT1-signaling by ZHX2 as analyzed by RQ-PCR and western blot. Taken together, we have identified a novel aberration with recurrent breakpoints in HL, t(4;8)(q27;q24), which activate PDE5A and repress ZHX2, deregulating apoptosis, differentiation, and STAT1-signaling in HL cells.
霍奇金/里德-斯滕伯格(HRS)细胞代表霍奇金淋巴瘤(HL)浸润淋巴结中的恶性成分。尽管 HRS 细胞显示出多种染色体异常,但很少有重现的,并且靶向基因未知。然而,了解 HL 的病理学并开发合理的治疗方法可能需要确定推定的失调基因。在这里,我们通过光谱核型分析分析了明确的 HL 细胞系 L-1236 的核型,并确定了多种异常,其中特别是 t(4;8)(q27;q24),其中包括先前在 HL 中强调的两个断点区域。通过高密度基因组阵列和荧光原位杂交对 4q27 和 8q24 的靶基因进行了短名单筛选。候选靶基因的表达分析显示,4q27 处的磷酸二酯酶 PDE5A 明显激活,8q24 处的同源盒基因 ZHX2 受到抑制。用 PDE5A 抑制剂西地那非或针对 PDE5A 的 siRNA 处理 L-1236,并同时用环鸟苷单磷酸(cGMP)刺激,导致细胞凋亡增加,表明 PDE5A 为癌基因。用 siRNA 介导的 ZHX2 敲低后对 L-1236 细胞进行表达谱分析显示,分化和凋亡调节基因受到抑制,表明 ZHX2 具有肿瘤抑制活性。下游基因包括 STAT1 和几个 STAT1 靶基因,表明 ZHX2 通过 RQ-PCR 和 Western blot 分析激活了 STAT1 信号。总之,我们已经确定了 HL 中具有重现断点的新型异常,t(4;8)(q27;q24),其激活 PDE5A 并抑制 ZHX2,使 HL 细胞中的凋亡、分化和 STAT1 信号失调。