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肿瘤抑制基因产物APC可阻止细胞周期从G0/G1期进入S期。

The tumour suppressor gene product APC blocks cell cycle progression from G0/G1 to S phase.

作者信息

Baeg G H, Matsumine A, Kuroda T, Bhattacharjee R N, Miyashiro I, Toyoshima K, Akiyama T

机构信息

Department of Oncogene Research, Osaka University, Japan.

出版信息

EMBO J. 1995 Nov 15;14(22):5618-25. doi: 10.1002/j.1460-2075.1995.tb00249.x.

DOI:10.1002/j.1460-2075.1995.tb00249.x
PMID:8521819
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC394677/
Abstract

The APC gene is mutated in familial adenomatous polyposis (FAP) as well as in sporadic colorectal tumours. The product of the APC gene is a 300 kDa cytoplasmic protein associated with the adherence junction protein catenin. Here we show that overexpression of APC blocks serum-induced cell cycle progression from G0/G1 to the S phase. Mutant APCs identified in FAP and/or colorectal tumours were less inhibitory and partially obstructed the activity of the normal APC. The cell-cycle blocking activity of APC was alleviated by the overexpression of cyclin E/CDK2 or cyclin D1/CDK4. Consistent with this result, kinase activity of CDK2 was significantly down-regulated in cells overexpressing APC although its synthesis remained unchanged, while CDK4 activity was barely affected. These results suggest that APC may play a role in the regulation of the cell cycle by negatively modulating the activity of cyclin-CDK complexes.

摘要

APC基因在家族性腺瘤性息肉病（FAP）以及散发性结直肠癌肿瘤中发生突变。APC基因的产物是一种300 kDa的细胞质蛋白，与黏附连接蛋白连环蛋白相关。在此我们表明，APC的过表达会阻断血清诱导的细胞周期从G0/G1期向S期的进展。在FAP和/或结直肠癌肿瘤中鉴定出的突变型APC抑制作用较弱，部分阻碍了正常APC的活性。细胞周期蛋白E/细胞周期蛋白依赖性激酶2（Cyclin E/CDK2）或细胞周期蛋白D1/细胞周期蛋白依赖性激酶4（Cyclin D1/CDK4）的过表达可减轻APC的细胞周期阻滞活性。与此结果一致，在过表达APC的细胞中，CDK2的激酶活性显著下调，尽管其合成保持不变，而CDK4活性几乎不受影响。这些结果表明，APC可能通过负向调节细胞周期蛋白 - 细胞周期蛋白依赖性激酶复合物的活性在细胞周期调控中发挥作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f47b/394677/112fe82d5884/emboj00046-0176-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f47b/394677/c67680d79f27/emboj00046-0173-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f47b/394677/dcea3ff98f12/emboj00046-0173-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f47b/394677/21a711cb3035/emboj00046-0174-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f47b/394677/b13a8c81fdd5/emboj00046-0175-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f47b/394677/b7014b60a384/emboj00046-0175-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f47b/394677/112fe82d5884/emboj00046-0176-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f47b/394677/c67680d79f27/emboj00046-0173-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f47b/394677/dcea3ff98f12/emboj00046-0173-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f47b/394677/21a711cb3035/emboj00046-0174-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f47b/394677/b13a8c81fdd5/emboj00046-0175-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f47b/394677/b7014b60a384/emboj00046-0175-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f47b/394677/112fe82d5884/emboj00046-0176-a.jpg

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