LaBiche R A, Demars M, Nicolson G L
Department of Tumor Biology, University of Texas M.D. Anderson Cancer Center, Houston 77030.
In Vivo. 1992 Jul-Aug;6(4):317-24.
The relative levels of mitochondrial specific gene transcripts were compared in two murine large cell lymphoma cell lines that differ in their propensities to form liver metastases and in their sensitivity to macrophage mediated antitumor cytostasis and cytolysis. Full-length transcripts of the mitochondrial genes were hybridized on electroblots from citrate/urea gels with specific gene prodes. The mitochondrially encoded gene NADH dehydrogenase subunit 5 (ND5), that encodes a component of NADH dehydrogenase (complex I) of the electron transport chain, was significantly overexpressed in the highly metastatic RAW117-H10 compared to low metastatic RAW117-P cells. Results from analysis of RNA blots were confirmed in an S1 nuclease protection assay. Since RAW117-H10 cells are significantly more resistant to cytostasis by activated macrophages in coculture and such macrophage activity can inhibit RAW117 tumor cell respiration and growth, a mechanism was suggested that allows RAW117 cell escape from certain host effector mechanisms that block cellular respiration by an increase in the in vivo concentrations of translatable messenger RNA (mRNA) that codes for key components of the electron transport chain.
在两种小鼠大细胞淋巴瘤细胞系中比较了线粒体特异性基因转录本的相对水平，这两种细胞系在形成肝转移的倾向以及对巨噬细胞介导的抗肿瘤细胞停滞和细胞溶解的敏感性方面存在差异。线粒体基因的全长转录本与特定基因探针在柠檬酸盐/尿素凝胶的电印迹上进行杂交。线粒体编码基因NADH脱氢酶亚基5（ND5）编码电子传递链中NADH脱氢酶（复合体I）的一个组分，与低转移性的RAW117 - P细胞相比，在高转移性的RAW117 - H10细胞中显著过表达。RNA印迹分析结果在S1核酸酶保护试验中得到证实。由于RAW117 - H10细胞在共培养中对活化巨噬细胞引起的细胞停滞具有显著更高的抗性，且这种巨噬细胞活性可抑制RAW117肿瘤细胞的呼吸和生长，因此提出了一种机制，即通过增加编码电子传递链关键组分的可翻译信使RNA（mRNA）的体内浓度，使RAW117细胞能够逃避某些阻断细胞呼吸的宿主效应机制。
