PLK1 has tumor-suppressive potential in APC-truncated colon cancer cells
作者： Monika Raab , Mourad Sanhaji , Yves Matthess , Albrecht Hörlin , Ioana Lorenz
DOI: 10.1038/S41467-018-03494-4
关键词:
摘要: The spindle assembly checkpoint (SAC) acts as a molecular safeguard in ensuring faithful chromosome transmission during mitosis, which is regulated by complex interplay between phosphatases and kinases including PLK1. Adenomatous polyposis coli (APC) germline mutations cause aneuploidy are responsible for familial adenomatous (FAP). Here we study the role of PLK1 colon cancer cells with chromosomal instability promoted APC truncation (APC-ΔC). expression APC-ΔC reduces accumulation mitotic upon inhibition, accelerates exit increases survival enhanced abnormalities. inhibition mitotic, APC-∆C-expressing kinetochore levels Aurora B hampers recruitment SAC component suggesting compromised checkpoint. Furthermore, Plk1 (RNAi, pharmacological compounds) promotes development polyps two independent Apc Min/+ mouse models. High patients expressing truncated significantly.
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