Kim Kwanghee, Brush James M, Watson Philip A, Cacalano Nicholas A, Iwamoto Keisuke S, McBride William H
Department of Radiation Oncology, David Geffen School of Medicine at University of California at Los Angeles, Los Angeles, CA 90095-1714, USA.
Mol Cancer Res. 2008 Mar;6(3):426-34. doi: 10.1158/1541-7786.MCR-07-0313.
Little is known about the factors that influence the proteasome structures in cells and their activity, although this could be highly relevant to cancer therapy. We have previously shown that, within minutes, irradiation inhibits substrate degradation by the 26S proteasome in most cell types. Here, we report an exception in U87 glioblastoma cells transduced to express the epidermal growth factor receptor vIII (EGFRvIII) mutant (U87EGFRvIII), which does not respond to irradiation with 26S proteasome inhibition. This was assessed using either a fluorogenic substrate or a reporter gene, the ornithine decarboxylase degron fused to ZsGreen (cODCZsGreen), which targets the protein to the 26S proteasome. To elucidate whether this was due to alterations in proteasome composition, we used quantitative reverse transcription-PCR to quantify the constitutive (X, Y, Z) and inducible 20S subunits (Lmp7, Lmp2, Mecl1), and 11S (PA28alpha and beta) and 19S components (PSMC1 and PSMD4). U87 and U87EGFRvIII significantly differed in expression of proteasome subunits, and in particular immunosubunits. Interestingly, 2 Gy irradiation of U87 increased subunit expression levels by 16% to 324% at 6 hours, with a coincident 30% decrease in levels of the proteasome substrate c-myc, whereas they changed little in U87EGFRvIII. Responses similar to 2 Gy were seen in U87 treated with a proteasome inhibitor, NPI0052, suggesting that proteasome inhibition induced replacement of subunits independent of the means of inhibition. Our data clearly indicate that the composition and function of the 26S proteasome can be changed by expression of the EGFRvIII. How this relates to the increased radioresistance associated with this cell line remains to be established.
虽然这可能与癌症治疗高度相关,但对于影响细胞中蛋白酶体结构及其活性的因素却知之甚少。我们之前已经表明,在大多数细胞类型中,照射在几分钟内就能抑制26S蛋白酶体对底物的降解。在此,我们报告了一个例外情况,即转导表达表皮生长因子受体vIII(EGFRvIII)突变体的U87胶质母细胞瘤细胞(U87EGFRvIII),其对照射不产生26S蛋白酶体抑制反应。这是通过使用荧光底物或报告基因(与ZsGreen融合的鸟氨酸脱羧酶降解结构域,cODCZsGreen)来评估的,该报告基因将蛋白质靶向26S蛋白酶体。为了阐明这是否是由于蛋白酶体组成的改变,我们使用定量逆转录PCR来定量组成型(X、Y、Z)和诱导型20S亚基(Lmp7、Lmp2、Mecl1),以及11S(PA28α和β)和19S组分(PSMC1和PSMD4)。U87和U87EGFRvIII在蛋白酶体亚基的表达上,特别是免疫亚基的表达上存在显著差异。有趣的是,2 Gy照射U87后,6小时时亚基表达水平增加了16%至324%,同时蛋白酶体底物c-myc的水平下降了30%,而在U87EGFRvIII中它们变化很小。在用蛋白酶体抑制剂NPI0052处理的U87中观察到了与2 Gy类似的反应,这表明蛋白酶体抑制诱导了亚基的替代,而与抑制方式无关。我们的数据清楚地表明,26S蛋白酶体的组成和功能可以因EGFRvIII的表达而改变。这与该细胞系增加的放射抗性如何相关仍有待确定。