Scott R E, Estervig D N, Tzen C Y, Minoo P, Maercklein P B, Hoerl B J
Section of Experimental Pathology, Mayo Clinic/Foundation, Rochester, MN 55905.
Proc Natl Acad Sci U S A. 1989 Mar;86(5):1652-6. doi: 10.1073/pnas.86.5.1652.
The potential of nonterminal cellular differentiation to stably repress the expression of the neoplastic phenotype of transformed cells is established. Nonterminal differentiation induces spontaneously transformed 3T3 T cells to revert to a nontransformed state and induces the revertant cell clones to become resistant to retransformation by UV irradiation or 4-nitroquinoline oxide treatment. Nonterminal differentiation also induces simian virus 40-transformed 3T3 T cells to repress expression of the large tumor antigen and to revert to a nontransformed state. Although the molecular mechanisms that mediate these and other forms of anticancer activity have not been definitively established, data are presented which suggest that differentiation-induced repression of large tumor antigen expression can be regulated at the level of transcription and/or RNA processing.
已证实非终末细胞分化具有稳定抑制转化细胞肿瘤表型表达的潜力。非终末分化可诱导自发转化的3T3 T细胞恢复至未转化状态,并诱导回复细胞克隆对紫外线照射或4-硝基喹啉氧化物处理产生再转化抗性。非终末分化还可诱导猿猴病毒40转化的3T3 T细胞抑制大肿瘤抗原的表达并恢复至未转化状态。尽管介导这些及其他形式抗癌活性的分子机制尚未明确确立,但现有数据表明,分化诱导的大肿瘤抗原表达抑制可在转录和/或RNA加工水平受到调控。