Cell surface glycolipids of transformed NIH 3T3 cells transfected with DNAs of human bladder and lung carcinomas.
Cell surface glycolipids of transformed NIH 3T3 cells transfected with DNAs of human bladder and lung carcinomas.
复制标题
转染人膀胱癌和肺癌 DNA 的转化 NIH 3T3 细胞的细胞表面糖脂。
DOI：
10.1002/j.1460-2075.1983.tb01741.x
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发表时间：
1983
期刊：
影响因子：
--
通讯作者：
Hakomori,S
中科院分区：
文献类型：
--
作者：
Tsuchiya,S;Hakomori,S
研究了转染人肺癌（Lx‐1）和人膀胱癌（Ej） dna介导的NIH 3T3细胞的中性糖脂和神经节苷。在转染Lx‐1或Ej癌细胞的dna转化的NIH 3T3细胞中，神经节三甲神经酰胺（gangliotriaosylceramide, Gg3）的化学量和细胞表面暴露程度都大大增加。在小鼠肉瘤病毒Kirsten株转化的BALB/c 3T3细胞中，Gg3的细胞表面暴露发生了相同但更明显的变化，但在原始的Lx‐1或Ej人癌中没有相同的糖脂。糖脂的化学量和组织机制受多种因素控制。这不仅包括糖基转移酶和水解酶在细胞膜上的数量，也包括它们的组织。这也涉及通过细胞骨架-膜连接调节的膜动力学，这可能决定细胞表面糖脂暴露的程度。Kirsten小鼠肉瘤病毒的3T3转化体与转染人类癌症dna的3T3转化体的糖脂Gg3的化学和组织变化相似，这可能表明致癌基因激活触发了共同的生化基础。
Neutral glycolipids and gangliosides of NIH 3T3 cells oncogenically transformed by transfection of DNAs from human lung carcinoma (Lx‐1) and human bladder carcinoma (Ej) have been investigated. The chemical quantity and the degree of cell surface exposure of gangliotriaosylceramide (Gg3) were greatly enhanced in NIH 3T3 cells transformed by transfection of DNAs of either Lx‐1 or Ej carcinoma cells. An identical but more conspicuous change in cell surface exposure of Gg3 was observed in BALB/c 3T3 cells transformed by murine sarcoma virus Kirsten strain, but the same glycolipid was absent in the original Lx‐1 or Ej human carcinomas. The mechanism that defines the chemical quantity and the organization of glycolipids is controlled by multiple factors. These include not only the quantity but also the organization of glycosyl transferases and hydrolases in membranes. This also involves membrane dynamics regulated through a cytoskeletal‐membrane conjunction which may determine the degree of glycolipid exposure at the cell surface. The similarity of the chemical and organizational change of a single glycolipid, Gg3, between 3T3 transformants by Kirsten murine sarcoma virus and those by transfection of human cancer DNAs may indicate a common biochemical basis triggered by activation of the oncogene.