PI3K/Akt/mTOR activation by suppression of ELK3 mediates chemosensitivity of MDA-MB-231 cells to doxorubicin by inhibiting autophagy
- Authors
- Park, Ji-Hoon; Kim, Keun Pil; Ko, Jeong-Jae; Park, Kyung-Soon
- Issue Date
- Aug-2016
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- Autophagy; Doxorubicin; ELK3; MDA-MB-231 cell line; PI3K/Akt
- Citation
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.477, no.2, pp 277 - 282
- Pages
- 6
- Journal Title
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
- Volume
- 477
- Number
- 2
- Start Page
- 277
- End Page
- 282
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/6633
- DOI
- 10.1016/j.bbrc.2016.06.057
- ISSN
- 0006-291X
1090-2104
- Abstract
- Drug resistance in breast cancer remains a major obstacle of clinical therapy. We found that suppression of ELK3 in the triple negative breast cancer cell line MDA-MB-231 impaired autophagy and led to a hypersensitive response to doxorubicin treatment. In ELK3-knockdown MDA-MB-231 cells (ELK3 KD), autophagy was not activated under starvation conditions, which is a major stimulus of autophagy activation. We revealed that activation of the PI3K/Akt pathway was the main cause of impaired autophagy in ELK3 KD. Our results suggest that targeting ELK3 may be a potential approach to overcome doxorubicin resistance in breast cancer therapeutics. (C) 2016 Published by Elsevier Inc.
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