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Cell Cycle–Dependent Ciliogenesis and Cancer

¹ Fox Chase Cancer Center, Philadelphia, Pennsylvania; ² Department of Molecular Biology and Medical Biotechnology, Russian State Medical University, Moscow, Russia; and ³ Department of Biochemistry, Mary Babb Randolph Cancer Center; and West Virginia University, School of Medicine, Morgantown, West Virginia

Requests for reprints: Elena N. Pugacheva, Department of Biochemistry, Mary Babb Randolph Cancer Center, West Virginia University, School of Medicine, Morgantown, WV 26506-9300. Phone: 304-293-5295; Fax: 304-293-4667; E-mail: epugacheva{at}hsc.wvu.edu.

Key Words: Cancer • cell cycle • cilia

In mammals, most cell types have primary cilia, protruding structures involved in sensing mechanical and chemical signals from the extracellular environment that act as major communication hubs for signaling controlling cell differentiation and polarity. The list of clinical disorders associated with ciliary dysfunction has expanded from polycystic kidney disease to include many others. Transformed cells commonly lack cilia, but whether this lack is cause or consequence of transformation is not well understood. Here we discuss work addressing recently identified actions of the cancer-promoting proteins Aurora A and HEF1/NEDD9/CAS-L at cilia. Together with older studies, this work suggests that loss of cilia in cancer may contribute to the insensitivity of cancer cells to environmental repressive signals, based in part on derangement of cell cycle checkpoints governed by cilia and centrosomes. [Cancer Res 2008;68(7):2058–61]

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