铜缺乏
铜
基因组
细胞
细胞生长
生物
癌症研究
医学
化学
遗传学
基因
有机化学
作者
Éric Renault,Jean Deschatrette
标识
DOI:10.1080/01635589709514631
摘要
Abstract Copper deficiency imposed on a variant rat hepatoma cell line inhibits cell growth and results in genesis of stable well‐differentiated, tumorigenic revertants. The treatment caused a substantial increase in DNA content (up to 20%) of G1 and G2/M cells and inhibition of cell proliferation. This phenomenon was correlated with an enhancement of DNA replication. The excess DNA was unstable and rapidly lost with reinitiation of cell growth and mitosis. Minute and double‐minute extrachromosomal material was detected by metaphase analysis, suggesting widespread DNA amplification in copper‐deficient conditions. Although transitory, these genetic events were associated with genesis of drug‐resistant cells and induction of tumorigenicity of the variant hepatoma cells. The data reveal a novel aspect of the consequences of trace element deficiency.
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