TOR complex 2 is needed for cell cycle progression and anchorage-independent growth of MCF7 and PC3 tumor cells
<p>Abstract</p> <p>Background</p> <p>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 phospho...
| Main Authors: | , |
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| Format: | Article |
| Language: | English |
| Published: |
BMC
2008-10-01
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| Series: | BMC Cancer |
| Online Access: | http://www.biomedcentral.com/1471-2407/8/282 |
| Summary: | <p>Abstract</p> <p>Background</p> <p>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.</p> <p>Methods</p> <p>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.</p> <p>Results</p> <p>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.</p> <p>Conclusion</p> <p>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.</p> |
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| ISSN: | 1471-2407 |