Human tripartite motif protein 52 is required for cell context-dependent proliferation
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Stefan Benke1, Benedikt Agerer1, Lisa Haas2, Martin Stöger1, Alexander Lercher3, Lisa Gabler4, Izabella Kiss1, Sara Scinicariello1, Walter Berger4, Andreas Bergthaler3, Anna C. Obenauf2 and Gijs A. Versteeg1
1Department of Microbiology, Immunobiology, and Genetics, Max F. Perutz Laboratories, University of Vienna, Vienna Biocenter, Vienna 1030, Austria
2Research Institute of Molecular Pathology, Vienna Biocenter, Vienna 1030, Austria
3CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna 1090, Austria
4Institute of Cancer Research and Comprehensive Cancer Center, Department of Medicine I, Medical University of Vienna, Vienna A-1090, Austria
Gijs A. Versteeg, email: email@example.com
Keywords: tripartite motif protein (TRIM); glioblastoma; proliferation; p53; glucose metabolism
Received: October 02, 2017 Accepted: January 30, 2018 Published: February 05, 2018
Tripartite motif (TRIM) proteins have been shown to play important roles in cancer development and progression by modulating cell proliferation or resistance from cell death during non-homeostatic stress conditions found in tumor micro-environments. In this study, we set out to investigate the importance for cellular fitness of the virtually uncharacterized family member TRIM52.
The human TRIM52 gene has arisen recently in evolution, making it unlikely that TRIM52 is required for basic cellular functions in normal cells. However, a recent genome-wide ablation screening study has suggested that TRIM52 may be essential for optimal proliferation or survival in certain genetic cancer backgrounds. Identifying genes which fit this concept of genetic context-dependent fitness in cancer cells is of interest as they are promising targets for tumor-specific therapy.
We report here that TRIM52 ablation significantly diminished the proliferation of specific glioblastoma cell lines in cell culture and mouse xenografts by compromising their cell cycle progression in a p53-dependent manner. Together, our findings point to a non-redundant TRIM52 function that is required for optimal proliferation.
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