Reversal of the temperature-shift-induced growth restriction of a temperature-sensitive simian virus 40 T-antigen-transformed human fibroblast cell line by treatment with retinoic acid.
Reversal of the temperature-shift-induced growth restriction of a temperature-sensitive simian virus 40 T-antigen-transformed human fibroblast cell line by treatment with retinoic acid.
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通过用视黄酸处理，逆转温度敏感的猿猴病毒 40 T 抗原转化的人成纤维细胞系的温度变化诱导的生长限制。
DOI：
10.1042/bj3170707
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
S. L. Chen
中科院分区：
文献类型：
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作者：
Y. Tsao;S. F. Li;S. Kuo;J. C. Liu;S. L. Chen
我们之前建立了一个人成纤维细胞系HFL 6-2，它含有一种温度敏感的猿猴病毒40（SV 40）T抗原，允许细胞在35 ℃生长，但限制在39 ℃生长。p21（Waf 1/Cip 1）在HFL 6-2细胞中被温度变化显著诱导。在这里，我们表明，全反式维甲酸（RA）处理防止HFL 6-2细胞在39摄氏度的生长限制。在RA存在下，HFL 6-2细胞甚至在39 ℃下也增殖成相当大的集落。[3 H]胸苷掺入和流式细胞术分析显示，暴露于RA的细胞在39 ℃下保持DNA合成。RA对生长受限的预防与在转录水平上缺乏p21的诱导相关。这些结果表明，RA可能通过抑制p21基因表达来阻止衰老过程，并干扰体细胞的生长调节。
We previously established a human fibroblast cell line, HFL 6-2, that contains a temperature sensitive simian virus 40 (SV40) T antigen, permitting cell growth at 35 degrees C but restricting growth at 39 degrees C. p21 (Waf1/Cip1) was significantly induced by temperature shifts in HFL 6-2 cells. Here we show that all-trans-retinoic acid (RA) treatment prevented the growth restriction of HFL 6-2 cells at 39 degrees C. In the presence of RA, HFL 6-2 cells proliferated into sizeable colonies even at 39 degrees C. [3H]Thymidine incorporation and flow cytometry analysis revealed that cells exposed to RA maintained DNA synthesis at 39 degrees C. Prevention of growth restriction by RA was correlated with a lack of induction of p21 at the transcription level. These observations suggest that RA may prevent the senescence process by repressing p21 gene expression, and perturb the growth regulation of somatic cells.