期刊
BMC CANCER
卷 8, 期 -, 页码 -出版社
BIOMED CENTRAL LTD
DOI: 10.1186/1471-2407-8-282
关键词
-
类别
资金
- Academy of Finland
- Helsingin Sanomain 100-vuotissaatio (Finland)
- Marie Curie Intra-European Fellowship
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 GI phase, and showed prominent downregulation of Cyclin DI. 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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据