Induction of tumorigenicity and lack of in vitro growth requirement for 12-O-tetradecanoylphorbol-13-acetate by transfection of murine melanocytes with v-Ha-ras.
Induction of tumorigenicity and lack of in vitro growth requirement for 12-O-tetradecanoylphorbol-13-acetate by transfection of murine melanocytes with v-Ha-ras.
复制标题
通过用 v-Ha-ras 转染小鼠黑色素细胞，诱导致瘤性并且缺乏 12-O-十四烷酰佛波醇-13-乙酸酯的体外生长要求。
作者：
R. Wilson;T. P. Dooley;I. Hart
小鼠黑色素细胞的非致瘤系 Mel-ab 已被莫洛尼小鼠白血病病毒长末端重复转录控制下的 v-Ha-ras 基因转染。转染子在受体小鼠中产生快速生长的未分化黑色素瘤。在体外和体内均可观察到转化细胞中黑色素产生的抑制表明 ras 可能影响黑素细胞的细胞分化。 Mel-ab 细胞需要持续存在 12-O-十四烷酰佛波醇-13-乙酸酯或其他蛋白激酶 C 激活剂才能进行体外生长。表达 v-Ha-ras 的转染子不再表现出这种要求，并且实际上通过添加蛋白激酶 C 激活剂来抑制生长。这些结果与 ras 通过蛋白激酶 C 途径发挥作用并赋予 Mel-ab 细胞自主生长的观点一致。
A nontumorigenic line of murine melanocytes, Mel-ab, has been transfected with the v-Ha-ras gene under transcriptional control of the Moloney murine leukemia virus long terminal repeat. Transfectants produced rapidly growing undifferentiated melanomas in recipient mice. The inhibition of melanin production in transformed cells, observable both in vitro and in vivo, suggests that ras may affect melanocyte cytodifferentiation. Mel-ab cells require the continual presence of 12-O-tetradecanoylphorbol-13-acetate, or other activators of protein kinase C, for in vitro growth. Transfectants expressing v-Ha-ras no longer manifested this requirement and were actually growth inhibited by the addition of protein kinase C activators. These results are consistent with the notion that ras acts via the protein kinase C pathway in conferring autonomous growth on Mel-ab cells.
SP1 小鼠乳腺癌细胞的转移潜力是由激活的和正常形式的 c-H-ras 诱导的。
影响因子：
8
作者：
Waghorne,C;Kerbel,RS;Breitman,ML
通讯作者：
Breitman,ML
DOI：
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发表时间：
1987-05
期刊：
Laboratory investigation; a journal of technical methods and pathology
影响因子：
--
作者：
M. Herlyn;W. Clark;U. Rodeck;M. Mancianti;J. Jambrosic;H. Koprowski
通讯作者：
M. Herlyn;W. Clark;U. Rodeck;M. Mancianti;J. Jambrosic;H. Koprowski