Journal
CANCER RESEARCH
Volume 68, Issue 7, Pages 2058-2061Publisher
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/0008-5472.CAN-07-5838
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Funding
- NATIONAL CANCER INSTITUTE [R01CA113342, P30CA006927, R01CA063366] Funding Source: NIH RePORTER
- NCI NIH HHS [CA06927, R01 CA63366, P30 CA006927, R01 CA113342-02, R01 CA113342, P30 CA006927-46, R01 CA063366, R01 CA063366-12] Funding Source: Medline
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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 REFI/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.
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