Browse

Suppression of mTOR via Akt-dependent and -independent mechanisms in selenium-treated colon cancer cells: involvement of AMPK alpha(1)

Cited 37 time in Web of Science Cited 42 time in Scopus
Authors
Lee, Yun-Kyoung; Park, Song Yi; Kim, Young-Min; Kim, Dong Chool; Lee, Won Sup; Surh, Young-Joon; Park, Ock Jin
Issue Date
2010-06
Citation
Carcinogenesis, Vol.31 No.6, pp.1092-1099
Abstract
Activation of the mammalian target of rapamycin (mTOR) pathway promotes tumorigenesis, and inhibiting the mammalian target of rapamycin complex 1 (mTORC1) has emerged as an attractive target for suppressing tumor growth. We found that selenium treatment of HT-29 colon cancer cells suppressed mTORC1 through Akt-independent and -dependent pathways. In Akt-independent mTORC1 inhibition in selenium-treated colon cancer cells, adenosine monophosphate-activated protein kinase (AMPK) alpha(1) was crucial for suppression of mTORC1 activity. In contrast, the Akt-dependent mTORC1 inhibition by selenium did not require AMPK alpha(1). The importance of the AMPK alpha(1)-mTORC1 pathway in mediating the antiproliferative action of selenium was examined in xenograft tumors, and the suppression of mTORC1 as well as Akt was concomitant with an increase in AMPK alpha(1) activity. These findings suggest that the antiproliferative effect of selenium is mediated by an Akt-independent AMPK alpha(1)/mTORC1 pathway or by the Akt/tuberous sclerosis complex 2 /mTORC1 pathway.
ISSN
0143-3334
URI
https://hdl.handle.net/10371/172814
DOI
https://doi.org/10.1093/carcin/bgq040
Files in This Item:
There are no files associated with this item.
Appears in Collections:
Graduate School of Convergence Science and Technology (융합과학기술대학원)Dept. of Molecular and Biopharmaceutical Sciences (분자의학 및 바이오제약학과)Journal Papers (저널논문_분자의학 및 바이오제약학과)
  • mendeley

Items in S-Space are protected by copyright, with all rights reserved, unless otherwise indicated.

Browse