PMID- 20164123
OWN - NLM
STAT- MEDLINE
DCOM- 20100624
LR  - 20211203
IS  - 1460-2180 (Electronic)
IS  - 0143-3334 (Linking)
VI  - 31
IP  - 6
DP  - 2010 Jun
TI  - Suppression of mTOR via Akt-dependent and -independent mechanisms in 
      selenium-treated colon cancer cells: involvement of AMPKalpha1.
PG  - 1092-9
LID - 10.1093/carcin/bgq040 [doi]
AB  - 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 AMPKalpha(1). The importance of the 
      AMPKalpha(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 AMPKalpha(1) activity. These findings suggest 
      that the antiproliferative effect of selenium is mediated by an Akt-independent 
      AMPKalpha(1)/mTORC1 pathway or by the Akt/tuberous sclerosis complex 2 /mTORC1 
      pathway.
FAU - Lee, Yun-Kyoung
AU  - Lee YK
AD  - Department of Food and Nutrition, Hannam University Daedeok Valley Campus, 
      Daejeon 305-811, Korea.
FAU - Park, Song Yi
AU  - Park SY
FAU - Kim, Young-Min
AU  - Kim YM
FAU - Kim, Dong Chool
AU  - Kim DC
FAU - Lee, Won Sup
AU  - Lee WS
FAU - Surh, Young-Joon
AU  - Surh YJ
FAU - Park, Ock Jin
AU  - Park OJ
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20100217
PL  - England
TA  - Carcinogenesis
JT  - Carcinogenesis
JID - 8008055
RN  - 0 (Intracellular Signaling Peptides and Proteins)
RN  - 0 (RNA, Small Interfering)
RN  - EC 2.7.1.1 (MTOR protein, human)
RN  - EC 2.7.1.1 (mTOR protein, mouse)
RN  - EC 2.7.11.1 (Protein Serine-Threonine Kinases)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - EC 2.7.11.31 (AMP-Activated Protein Kinases)
RN  - H6241UJ22B (Selenium)
SB  - IM
MH  - AMP-Activated Protein Kinases/*metabolism
MH  - Animals
MH  - Blotting, Western
MH  - Cell Proliferation
MH  - Colonic Neoplasms/enzymology/*metabolism/pathology
MH  - Enzyme Activation
MH  - HT29 Cells
MH  - Humans
MH  - Immunohistochemistry
MH  - Intracellular Signaling Peptides and Proteins/*antagonists & inhibitors
MH  - Male
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Nude
MH  - Phosphorylation
MH  - Protein Serine-Threonine Kinases/*antagonists & inhibitors
MH  - Proto-Oncogene Proteins c-akt/*metabolism
MH  - RNA, Small Interfering
MH  - Selenium/*pharmacology
MH  - TOR Serine-Threonine Kinases
EDAT- 2010/02/19 06:00
MHDA- 2010/06/25 06:00
CRDT- 2010/02/19 06:00
PHST- 2010/02/19 06:00 [entrez]
PHST- 2010/02/19 06:00 [pubmed]
PHST- 2010/06/25 06:00 [medline]
AID - bgq040 [pii]
AID - 10.1093/carcin/bgq040 [doi]
PST - ppublish
SO  - Carcinogenesis. 2010 Jun;31(6):1092-9. doi: 10.1093/carcin/bgq040. Epub 2010 Feb 
      17.