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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Sun, Ying Pooya, Shabnam Yachyshin, Sara Quinn, Brian Grabowski, Gregory A. Norga, Koenraad Viollet, Benoit Wortman, Matthew Warnick, Ronald E. Zhou, Xuan Mcpherson, Christopher Kendler, Ady Poels, Jeroen Giri, Shailendra Dasgupta, Biplab Liu, Xiaona Chhipa, Rishi Raj Chow, Lionel M. L. Kumar, Ashish |
| Description | Author Affiliation: Liu X ( Departments of Oncology, Experimental Hematology and Cancer Biology, and Human Genetics, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45242.); |
| Abstract | The multifunctional AMPK-activated protein kinase (AMPK) is an evolutionarily conserved energy sensor that plays an important role in cell proliferation, growth, and survival. It remains unclear whether AMPK functions as a tumor suppressor or a contextual oncogene. This is because although on one hand active AMPK inhibits mammalian target of rapamycin (mTOR) and lipogenesis--two crucial arms of cancer growth--AMPK also ensures viability by metabolic reprogramming in cancer cells. AMPK activation by two indirect AMPK agonists AICAR and metformin (now in over 50 clinical trials on cancer) has been correlated with reduced cancer cell proliferation and viability. Surprisingly, we found that compared with normal tissue, AMPK is constitutively activated in both human and mouse gliomas. Therefore, we questioned whether the antiproliferative actions of AICAR and metformin are AMPK independent. Both AMPK agonists inhibited proliferation, but through unique AMPK-independent mechanisms and both reduced tumor growth in vivo independent of AMPK. Importantly, A769662, a direct AMPK activator, had no effect on proliferation, uncoupling high AMPK activity from inhibition of proliferation. Metformin directly inhibited mTOR by enhancing PRAS40's association with RAPTOR, whereas AICAR blocked the cell cycle through proteasomal degradation of the G2M phosphatase cdc25c. Together, our results suggest that although AICAR and metformin are potent AMPK-independent antiproliferative agents, physiological AMPK activation in glioma may be a response mechanism to metabolic stress and anticancer agents. |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 4 |
| Volume Number | 111 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2014-01-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Cell Cycle Physiology Protein Kinases Drug Effects TOR Serine-Threonine Kinases Animals Brain Neoplasms Enzymology Metabolism Pathology Cell Proliferation Cells, Cultured Glioblastoma Lipogenesis Metformin Pharmacology Mice Mice, Knockout Genetics Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Multidisciplinary |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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