Regulation of the tumour suppressors APC and BRCA1 by nuclear export

癌细胞缺乏控制自身生长的能力，因此在局部环境中不断分裂，导致肿瘤形成。肿瘤抑制蛋白，如APC和BRCA1，通常作为调节剂发挥作用，帮助细胞对外界信号做出反应，并在必要时停止生长。肿瘤抑制蛋白的失活和改变的细胞定位可以促进癌症的发展。我们已经发现APC和BRCA1蛋白，其失活分别导致结肠癌和乳腺癌的发展，包含决定其在细胞内运动的信号。我们新的初步发现表明，APC和BRCA 1能够进出细胞核。我们的目标是确定这是如何发生的，并检查它们的细胞位置的调节如何影响这些抑癌蛋白的正常功能。最后，APC或BRCA 1的核通道异常可能解释它们在癌细胞中改变的细胞位置。

Cancer cells lack the ability to control their own growth, and thus continously divide in their local environment, leading to tumour formation. Tumour suppressor proteins, like APC and BRCA1, normally function as regulators to help cells respond to outside signals and to stop growing when necessary. The inactivation and altered cellular localisation of tumour suppressor proteins can contribute to cancer development. We have found that the APC and BRCA1 proteins, whose inactivation leads to development of colon cancer and breast cancer, respectively, contain signals that dictate their movement within the cell. Our novel preliminary findings reveal that APC and BRCA1 are able to move in and out of the cell nucleus. We aim to define how this occurs, and examine how the regulation of their cellular location affects the normal function of these cancer-suppressing proteins. Finally, abnormalities in the nuclear passage of APC or BRCA1 might explain their altered cellular location in cancer cells.