PMID- 24677093
OWN - NLM
STAT- MEDLINE
DCOM- 20150409
LR  - 20211203
IS  - 1521-4184 (Electronic)
IS  - 0365-6233 (Linking)
VI  - 347
IP  - 7
DP  - 2014 Jul
TI  - Role of AMP-activated protein kinase in cancer therapy.
PG  - 457-68
LID - 10.1002/ardp.201300402 [doi]
AB  - Recent advances in AMP-activated protein kinase (AMPK) as a target in cancer 
      waxed and waned over the past decade of cancer research. AMPK is a cellular 
      energy sensor, present in almost all eukaryotic cells. An elevated AMP/ATP ratio 
      activates the AMPK, which in turn inhibits energy-consuming processes and induces 
      catabolic events that generate ATP to restore the energy homeostasis inside the 
      cell. Several reports have indicated that AMPK regulates several metabolic 
      pathways and may be a potential therapeutic target for the treatment of cancer. 
      Cancer cells have specific metabolic changes that differ from normal cells, and 
      AMPK prevents the deregulated processes in cancer. AMPK may also act to inhibit 
      tumor formation through modulation of cell growth, cell proliferation, autophagy, 
      stress responses, and cell polarity. AMPK has been shown to inhibit mammalian 
      target of rapamycin (mTOR) through tuberous sclerosis complex 2 (TSC2) 
      phosphorylation and phosphatase and tensin homolog (PTEN), considered as central 
      cell growth controller signals in diseases. In response to glucose deprivation, 
      AMPK phosphorylates and activates p53, which induces cell cycle arrest in the 
      G1/S phase of the cell cycle. AMPK has also been reported to block 
      cyclin-dependent kinases through phosphorylation of p27(kip1) , promoting its 
      stabilization and allowing cells to survive metabolic stress via induction of 
      autophagy. Additionally, AMPK induces autophagy by phosphorylation and activation 
      of eEF-2 kinase, and prevents the formation of new proteins. AMPK activators are 
      also used for the treatment of type II diabetes and cancer. This review focuses 
      on AMPK activation and its possible therapeutic role in the treatment of cancer.
CI  - (c) 2014 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
FAU - Rehman, Gauhar
AU  - Rehman G
AD  - School of Life Science, College of Natural Science, Kyungpook National 
      University, Daegu, South Korea; Department of Zoology, Abdul Wali Khan 
      University, Mardan, K. P. K. Pakistan.
FAU - Shehzad, Adeeb
AU  - Shehzad A
FAU - Khan, Abdul Latif
AU  - Khan AL
FAU - Hamayun, Muhammad
AU  - Hamayun M
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20140328
PL  - Germany
TA  - Arch Pharm (Weinheim)
JT  - Archiv der Pharmazie
JID - 0330167
RN  - 0 (Tumor Suppressor Protein p53)
RN  - EC 2.7.1.1 (MTOR protein, human)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - EC 2.7.11.31 (AMP-Activated Protein Kinases)
SB  - IM
MH  - AMP-Activated Protein Kinases/*metabolism
MH  - Apoptosis
MH  - Autophagy
MH  - Humans
MH  - *Molecular Targeted Therapy/methods
MH  - Neoplasms/*drug therapy/enzymology/*metabolism/pathology
MH  - Phosphorylation
MH  - TOR Serine-Threonine Kinases/metabolism
MH  - Tumor Suppressor Protein p53/metabolism
OTO - NOTNLM
OT  - AMPK
OT  - Autophagy
OT  - Cancer
OT  - LKB1
OT  - mTORC1
EDAT- 2014/03/29 06:00
MHDA- 2015/04/10 06:00
CRDT- 2014/03/29 06:00
PHST- 2013/10/24 00:00 [received]
PHST- 2014/01/23 00:00 [revised]
PHST- 2014/01/31 00:00 [accepted]
PHST- 2014/03/29 06:00 [entrez]
PHST- 2014/03/29 06:00 [pubmed]
PHST- 2015/04/10 06:00 [medline]
AID - 10.1002/ardp.201300402 [doi]
PST - ppublish
SO  - Arch Pharm (Weinheim). 2014 Jul;347(7):457-68. doi: 10.1002/ardp.201300402. Epub 
      2014 Mar 28.