| Original language | English |
|---|---|
| Pages (from-to) | 547-548 |
| Number of pages | 2 |
| Journal | Autophagy |
| Volume | 7 |
| Issue number | 5 |
| DOIs | |
| Publication status | Published - May 2011 |
Bibliographical note
Funding Information:-BOEFT#JPTDJFODF inhibition of AMPK induces activation in many cancer cells. To investigate this ing potential of AEG-1 under metabolic of mTOR and S6K, and inactivation of hypothesis, we developed shAEG-1-T98G stress and apoptosis-deficient conditions. TSC1 followed by a decrease in ATG5 cells, a stable AEG-1 knockdown clone expression and finally a decrease in auto-in T98G, a human malignant glioma Acknowledgements phagy. Taken together, thi%s study pProvideOs cePll lineU, and EobseJrvTed thUat SshAJEGC-1-VThe pUreFsent study was supported in part relevant insights into the complex nature T98G cells have decreased accumulation by National Institutes of Health grant of AMPK and downstream responses that of LC3-II as compared to control T98G R01 CA134721, the Samuel Waxman may be involved in AEG-1-induced pro-cells, confirmed by confocal microscopy Cancer Research Foundation (SWCRF) tective autophagy and cancer progression. and western blotting. Autophagy provides and the National Foundation for Cancer Next, we investigated the physiologi-resistance to therapy-mediated tumor cell Research (NFCR) (P.B.F.); National cal role of protective autophagy induced death. When tumor cells induce protec-Cancer Institute Grant R01 CA138540, by AEG-1 in mediating cell survival. tive autophagy, inhibition of autophagy the Dana Foundation, and the Goldhirsh Our previous studies demonstrated that could provide a way of sensitizing tumor Foundation for Brain Cancer Research AEG-1 induces serum-independent cell cells to therapy by activating apoptosis. In (D.S.); and Korea Ministry of Education, growth, another property of oncogenic this recent paper, we demonstrate that che-Science and Technology through NRF transformation, by inhibiting apoptosis. moresistance promoted by AEG-1 may be (2009-0063466) (S.G.L.). D.S. is the To investigate the role of AEG-1-induced mediated through the ability of this gene Harrison Endowed Scholar in Cancer autophagy in regulating survival of normal to induce protective autophagy. Our study Research in the VCU Massey Cancer cells under serum starvation conditions, indicated that inhibition of AEG-1 results Center. P.B.F. holds the Thelma Newmeyer we analyzed cell survival by standard in a decrease in protective autophagy and Corman Chair in Cancer Research in MTT assays of Ad.AEG-1-infected causes chemosensitization of cancer cells. the VCU Massey Cancer Center and is a ATG5-deficient IM-PHFA cells grown in To determine whether AEG-1-induced SWCRF and NFCR Investigator.
Keywords
- AEG-1
- AMPK
- ATG5
- Protective autophagy