Schweigerer L, Scheurich P, Fotsis T
Sektion Onkologie/Immunologie, Universität-Kinderklinik Ruprecht-Karls-Universität, Heidelberg, FRG.
Biochem Biophys Res Commun. 1990 Aug 16;170(3):1301-7. doi: 10.1016/0006-291x(90)90535-u.
Human neuroblastoma cells with normal expression of the endogenous MYCN oncogene were transfected with a vector containing an exogenous MYCN gene. The transfected cells expressed the exogenous MYCN at high levels and had acquired a phenotype resembling that of cells from advanced human neuroblastomas. Proliferation of the MYCN-transfected, but not of the untransfected, neuroblastoma cells was inhibited by low concentrations of recombinant human tumor necrosis factor alpha (TNF alpha). Our results suggest that TNF alpha could be useful for the treatment of advanced human neuroblastomas, in which high MYCN expression seems to be a causative factor.
将含有外源性MYCN基因的载体转染到内源性MYCN癌基因表达正常的人神经母细胞瘤细胞中。转染后的细胞高水平表达外源性MYCN,并获得了类似于晚期人类神经母细胞瘤细胞的表型。低浓度的重组人肿瘤坏死因子α(TNFα)可抑制转染MYCN的神经母细胞瘤细胞的增殖,但不能抑制未转染细胞的增殖。我们的结果表明,TNFα可能对晚期人类神经母细胞瘤的治疗有用,其中MYCN的高表达似乎是一个致病因素。