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

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.

journal_name

Mol Cell Biol

authors

Schuendeln MM,Piekorz RP,Wichmann C,Lee Y,McKinnon PJ,Boyd K,Takahashi Y,Ihle JN

doi

10.1128/MCB.24.14.6403-6409.2004

subject

Has Abstract

pub_date

2004-07-01 00:00:00

pages

6403-9

issue

14

eissn

0270-7306

issn

1098-5549

pii

24/14/6403

journal_volume

24

pub_type

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