Induction of supermelanin synthesis and morphological changes in interspecific reconstituted cells and its reversal by tumor promoter.

T Sekiguchi, M Tosu, M C Yoshida, A Oikawa, K Ishihara, H Fujiki, M Tumuraya, T Kameya
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引用次数: 17

Abstract

Chloramphenicol-resistant (CAPr) reconstituted cells and cybrids were isolated by fusion of karyoplasts (or intact cells) of mouse amelanotic melanoma B16 cells with cytoplasts of hypoxanthine-guanine phosphoribosyltransferase (HGPRT) -deficient, CAPr rat myoblastic cells, L6TG.CAPr, and double selection in HAT medium containing CAP. Reconstituted cells or cybrids exhibited unique cellular arrangement, and about one third of the isolated clones expressed high tyrosinase activity and marked melanin synthesis, although the parental mouse cells expressed low tyrosinase activity and the parental rat cells did not express tyrosinase activity. These phenotypic changes have been stable for more than a year. The phenotypic reversions of these clonal cells were induced by treatment with a tumor promoter. There were changes in the morphology of the treated cells to that of the mouse B16 cells and extinction of tyrosinase activity and melanin synthesis in pigmented clonal cells. These phenotypic changes and reversions induced by a promoter were repeatedly reversible.

肿瘤启动子诱导种间重组细胞超黑色素合成和形态改变及其逆转。
将小鼠无色素黑色素瘤B16细胞核体(或完整细胞)与次黄嘌呤-鸟嘌呤磷酸核糖基转移酶(HGPRT)缺失的大鼠成肌细胞L6TG细胞质融合,分离出耐氯霉素(CAPr)重组细胞和细胞系。重组细胞或杂交体表现出独特的细胞排列,约三分之一的分离克隆表达高酪氨酸酶活性和显著的黑色素合成,尽管亲本小鼠细胞表达低酪氨酸酶活性,亲本大鼠细胞不表达酪氨酸酶活性。这些表型变化已经稳定了一年多。这些克隆细胞的表型逆转是由肿瘤启动子诱导的。处理后的细胞形态与小鼠B16细胞的形态发生变化,色素克隆细胞酪氨酸酶活性和黑色素合成消失。这些由启动子诱导的表型变化和逆转是反复可逆的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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