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The activation of TC10, a Rho small GTPase, contributes to v-Rel-mediated transformation

Oncogene volume 26, pages 2318–2329 (2007)Cite this article

Abstract

v-Rel is the oncogenic member of the Rel/NF-κB family of transcription factors and transforms hematopoietic cells and fibroblasts. Differential display was employed to identify target genes that exhibit altered expression in v-Rel transformed cells. One of the cDNAs identified encodes the chicken ortholog of TC10, a member of the Rho small GTPase family. The expression of TC10 was increased in v-Rel-transformed chicken embryonic fibroblasts (CEFs) 3 to 6-fold relative to control cells at both the RNA and protein levels. An elevated level of active, GTP-bound TC10 was also detected in v-Rel-transformed cells relative to control cells. Expression of a dominant-negative TC10 mutant (TC10T32N) decreased the colony formation potential of v-Rel-transformed cells. Furthermore, overexpression of wild-type TC10 or a gain-of-function mutant (TC10Q76L) greatly enhanced the ability of v-Rel transformed CEFs to form colonies in soft agar. In addition to enhance the transformation potential of v-Rel, the overexpression of wild-type TC10 or the gain-of-function mutant alone enhanced the saturation density of CEFs and was sufficient for their anchorage-independent growth in vitro. These results indicate that elevated TC10 activity contributes to v-Rel-mediated transformation of CEFs and demonstrate for the first time that a Rho factor alone is capable of inducing the in vitro transformation of primary cells.

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Acknowledgements

This study was supported by Public Health Service grants CA33192 from the National Cancer Institute.

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  1. M You

    Present address: Department of Hematopathology, Division of Pathology and Laboratory Medicine, UT M.D. Anderson Cancer Center, 1515 Holcombe Boulevard-Unit 72, Houston, TX, 77030, USA

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    S Tong, A S Liss, M You & H R Bose Jr

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Tong, S., Liss, A., You, M. et al. The activation of TC10, a Rho small GTPase, contributes to v-Rel-mediated transformation. Oncogene 26, 2318–2329 (2007). https://doi.org/10.1038/sj.onc.1210023

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