The centrosomal, putative tumor suppressor protein TACC2 is dispensable for normal development, and deficiency does not lead to cancer

Molecular and Cellular Biology
Michael M SchuendelnJames N Ihle

Abstract

TACC2 is a member of the transforming acidic coiled-coil-containing protein family and is associated with the centrosome-spindle apparatus during cell cycling. In vivo, the TACC2 gene is expressed in various splice forms predominantly in postmitotic tissues, including heart, muscle, kidney, and brain. Studies of human breast cancer samples and cell lines suggest a putative role of TACC2 as a tumor suppressor protein. To analyze the physiological role of TACC2, we generated mice lacking TACC2. TACC2-deficient mice are viable, develop normally, are fertile, and lack phenotypic changes compared to wild-type mice. Furthermore, TACC2 deficiency does not lead to an increased incidence of tumor development. Finally, in TACC2-deficient embryonic fibroblasts, proliferation and cell cycle progression as well as centrosome numbers are comparable to those in wild-type cells. Therefore, TACC2 is not required, nonredundantly, for mouse development and normal cell proliferation and is not a tumor suppressor protein.

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Citations

Apr 30, 2013·Cancer Letters·Geun-Hyoung HaEun-Kyoung Yim Breuer
Jun 15, 2014·Human Molecular Genetics·Kristen S PurringtonFergus J Couch
Jul 29, 2008·Trends in Cell Biology·Isabel Peset, Isabelle Vernos
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Aug 13, 2009·Journal of Cell Science·Shuchin TeiMitsuyoshi Nakao

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