Please use this identifier to cite or link to this item: https://doi.org/10.1186/1471-2407-8-282
Title: TOR complex 2 is needed for cell cycle progression and anchorage-independent growth of MCF7 and PC3 tumor cells
Authors: Hietakangas, V.
Cohen, S.M. 
Issue Date: 3-Oct-2008
Citation: Hietakangas, V., Cohen, S.M. (2008-10-03). TOR complex 2 is needed for cell cycle progression and anchorage-independent growth of MCF7 and PC3 tumor cells. BMC Cancer 8 : -. ScholarBank@NUS Repository. https://doi.org/10.1186/1471-2407-8-282
Abstract: Background: AKT signaling promotes cell growth, proliferation and survival and is hyperactivated in many cancers. TOR complex 2 (TORC2) activates AKT by phosphorylating it on the 'hydrophobic motif' site. Hydrophobic motif site phosphorylation is needed only for a subset of AKT functions. Whether proliferation of tumor cells depends on TORC2 activity has not been thoroughly explored. Methods: We used RNAi-mediated knockdown of rictor to inhibit TORC2 activity in MCF7 and PC3 tumor cells to analyze the importance of TORC2 on proliferation of tumor cells. Results: TORC2 inhibition reduced proliferation and anchorage-independent growth of both cell lines. Rictor depleted cells accumulated G1 phase, and showed prominent downregulation of Cyclin D1. Conclusion: This study provides further evidence that inhibition of TORC2 activity might be a useful strategy to inhibit proliferation of tumor cells and subsequent tumor growth. © 2008 Hietakangas and Cohen; licensee BioMed Central Ltd.
Source Title: BMC Cancer
URI: http://scholarbank.nus.edu.sg/handle/10635/130041
ISSN: 14712407
DOI: 10.1186/1471-2407-8-282
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