Zhong W, Oberley L W, Oberley T D, St Clair D K
Radiation Research Laboratory, The University of Iowa, Iowa City 52242, USA.
Oncogene. 1997 Jan 30;14(4):481-90. doi: 10.1038/sj.onc.1200852.
Manganese superoxide dismutase (MnSOD) has been previously shown to suppress the malignant phenotype of human melanoma and breast cancer cells. To test the possible role of MnSOD in glioma malignancy, MnSOD was overexpressed in wild type human glioma U118 cells and subcloned U118-9 cells by transfection of human MnSOD cDNA. The MnSOD-transfected cell lines demonstrated expression of exogenous (plasmid) MnSOD mRNA, increase in MnSOD immunoreactive protein, and a three- to eightfold increase in MnSOD enzymatic activity. The MnSOD overexpressing cell lines became less malignant as demonstrated by requiring a higher serum concentration to grow in vitro and much slower tumor growth in nude mice than the parental and neo control cell lines. These findings further support the hypothesis that MnSOD may be a tumor suppressor gene in a wide variety of human tumors.
先前已证明锰超氧化物歧化酶（MnSOD）可抑制人黑色素瘤和乳腺癌细胞的恶性表型。为了测试MnSOD在胶质瘤恶性肿瘤中的可能作用，通过转染人MnSOD cDNA，在野生型人胶质瘤U118细胞和亚克隆的U118 - 9细胞中过表达MnSOD。MnSOD转染的细胞系显示出外源（质粒）MnSOD mRNA的表达、MnSOD免疫反应性蛋白的增加以及MnSOD酶活性增加三至八倍。与亲本细胞系和新霉素对照细胞系相比，过表达MnSOD的细胞系恶性程度降低，这表现为在体外生长需要更高的血清浓度，并且在裸鼠中的肿瘤生长要慢得多。这些发现进一步支持了MnSOD可能是多种人类肿瘤中的肿瘤抑制基因这一假说。
