Beta-catenin and cyclin D1: connecting development to breast cancer.
Beta-catenin and cyclin D1: connecting development to breast cancer.
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发表时间：
2004
期刊：
影响因子：
4.3
通讯作者：
T. Rowlands;Irina V Pechenkina;S. Hatsell;P. Cowin
中科院分区：
文献类型：
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作者：
T. Rowlands;Irina V Pechenkina;S. Hatsell;P. Cowin
β -连环蛋白和细胞周期蛋白D1因其在人类癌症中的原致癌作用而引起了相当大的关注。在结肠癌细胞中发现cyclin D1是β -catenin的直接靶基因，这使得人们假设cyclin D1的上调对β -catenin的致癌性至关重要。我们最近的论文表明，情况并非如此；cyclin D1抑制活化的β -连环蛋白（mmtv - dn89β -连环蛋白）的致癌性。β -连环蛋白和细胞周期蛋白D1之间的关系和依赖性表明，它们在肺泡形成过程中起着不同的、必要的和连续的作用。这些结果支持了β -连环蛋白和周期蛋白D1的作用比细胞周期时钟的简单加速更为复杂的概念。这些蛋白质在涉及细胞命运决定的关键时刻被使用，我们推测需要特定类型的细胞周期来穿越。
Beta-catenin and cyclin D1 have attracted considerable attention due to their proto-oncogenic roles in human cancer. The finding of cyclin D1 as a direct target gene of beta-catenin in colon cancer cells led to the assumption that cyclin D1 upregulation is pivotal to beta-catenin's oncogenicity. Our recent paper shows that this is not the case; cyclin D1 dampens the oncogenicity of activated beta-catenin (MMTV-DN89beta-catenin). The relationships and dependencies of beta-catenin and cyclin D1 point to distinct, essential and sequential roles during alveologenesis. These results support the concept that both beta-catenin's and cyclin D1's actions are more sophisticated than simple acceleration of the cell cycle clock. These proteins are employed at critical junctures involving cell fate decisions that we speculate require specific types of cell cycle to traverse.