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通过跳过G1期限制点实现氧化还原介导的限制点旁路。

Redox-mediated bypass of restriction point via skipping of G1pm.

作者信息

Hoffman Arnold, Greene James J, Spetner Lee M, Burke Michael

机构信息

Redoxia, Jerusalem, Israel.

出版信息

Theor Biol Med Model. 2006 Jul 25;3:26. doi: 10.1186/1742-4682-3-26.

Abstract

BACKGROUND

It is well known that cancer cells bypass the restriction point, R, and undergo uncontrolled cell proliferation.

HYPOTHESIS AND EVIDENCE

We suggest here that fibrosarcoma cells enter G1ps directly from M, skipping G1pm, hence bypassing R, in response to redox modulation. Evidence is presented from the published literature that demonstrate a shortening of the cycle period of transformed fibroblasts (SV-3T3) compared to the nontransformed 3T3 fibroblasts, corresponding to the duration of G1pm in the 3T3 fibroblasts. Evidence is also presented that demonstrate that redox modulation can induce the CUA-4 fibroblasts to bypass R, resulting in a cycle period closely corresponding to the cycle period of fibrosarcoma cells (HT1080).

CONCLUSION

The evidence supports our hypothesis that a low internal redox potential can cause fibrosarcoma cells to skip the G1pm phase of the cell cycle.

摘要

背景

众所周知,癌细胞绕过限制点R,进行不受控制的细胞增殖。

假设与证据

我们在此提出,成纤维肉瘤细胞从M期直接进入G1ps期,跳过G1pm期,从而绕过R点,这是对氧化还原调节的反应。已发表文献中的证据表明,与未转化的3T3成纤维细胞相比,转化的成纤维细胞(SV - 3T3)的细胞周期缩短,这与3T3成纤维细胞中G1pm期的持续时间相对应。还有证据表明,氧化还原调节可诱导CUA - 4成纤维细胞绕过R点,导致其细胞周期与成纤维肉瘤细胞(HT1080)的细胞周期密切对应。

结论

这些证据支持我们的假设,即低细胞内氧化还原电位可导致成纤维肉瘤细胞跳过细胞周期的G1pm期。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ad0/1557840/36c67478878e/1742-4682-3-26-1.jpg

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