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CENP ‐R is a component of the  CENP ‐O complex, including  CENP ‐O,  CENP ‐P,  CENP ‐Q,  CENP ‐R, and  CENP ‐U and is constitutively localized to kinetochores throughout the cell cycle in vertebrates.  CENP ‐R‐deficient chicken  DT 40 cells are viable and show a very minor effect on mitosis. To investigate the functional roles of  CENP ‐R  in vivo , we generated  CENP ‐R‐deficient mice ( Cenp ‐ r  −/− ). Mice heterozygous or homozygous for  Cenp‐r  null mutation are viable and healthy, with no apparent defect in growth and morphology, indicating  Cenp‐r  is not essential for normal development. Accordingly, to investigate the role of the  Cenp‐r  gene in skin carcinogenesis, we subjected  Cenp ‐ r  −/−  mice to the 7,12‐dimethylbenz(a)anthracene ( DMBA )/ TPA  chemical carcinogenesis protocol and monitored tumor development. As a result,  Cenp ‐ r  −/−  mice initially developed significantly more papillomas than control wild‐type mice. However, papillomas in  Cenp ‐ r  −/−  mice showed a decrease of proliferative cells and an increase of apoptotic cells. As a result, they did not grow bigger and some papillomas showed substantial regression. Furthermore, papillomas in  Cenp ‐ r  −/−  mice showed lower frequency of malignant conversion to squamous cell carcinomas. These results indicate  Cenp‐r  functions bilaterally in cancer development: during early developmental stages,  Cenp‐r  functions as a tumor suppressor, but during the expansion and progression of papillomas it functions as a tumor‐promoting factor.

CENP ‐R acts bilaterally as a tumor suppressor and as an oncogene in the two‐stage skin carcinogenesis model