PMID- 29730477
OWN - NLM
STAT- MEDLINE
DCOM- 20181126
LR  - 20181126
IS  - 1476-5586 (Electronic)
IS  - 1522-8002 (Print)
IS  - 1476-5586 (Linking)
VI  - 20
IP  - 6
DP  - 2018 Jun
TI  - eIF4E Phosphorylation in Prostate Cancer.
PG  - 563-573
LID - S1476-5586(18)30001-0 [pii]
LID - 10.1016/j.neo.2018.04.003 [doi]
AB  - Prostate cancer (PCa) progression involves a shift from endocrine to paracrine 
      and eventually autocrine control resulting from alterations in molecular 
      mechanisms in the cells. Deregulation of RNA translation is crucial for tumor 
      cells to grow and proliferate; therefore, overactivation of the translation 
      machinery is often observed in cancer. The two most important signal transduction 
      pathways regulating PCa progression are PI3K/Akt/mTOR and Ras/MAPK. These two 
      pathways converge on the eukaryotic translation initiation factor 4E (eIF4E) 
      which binds to the protein scaffold eIF4G upon mechanistic target of rapamycin 
      (mTOR) activation and is phosphorylated by the mitogen-activated protein kinase 
      (MAPK) interacting protein kinases (Mnk1/2). This review describes the role of 
      eIF4E in mRNA translation initiation mediated by its binding to the methylated 5' 
      terminal structure (m7G-cap) of many mRNAs, and the ability of many tumor cells 
      to bypass this mechanism. Hormonal therapy and chemotherapy are two of the most 
      prevalent therapies used in patients with advanced PCa, and studies have 
      implicated a role for eIF4E phosphorylation in promoting resistance to both these 
      therapies. It appears that eIF4E phosphorylation enhances the rate of translation 
      of oncogene mRNAs to increase tumorigenicity.
CI  - Published by Elsevier Inc.
FAU - D'Abronzo, Leandro S
AU  - D'Abronzo LS
AD  - VA Northern California Health Care System, Mather, CA; Department of Urological 
      Surgery, University of California at Davis, Sacramento, CA.
FAU - Ghosh, Paramita M
AU  - Ghosh PM
AD  - VA Northern California Health Care System, Mather, CA; Department of Urological 
      Surgery, University of California at Davis, Sacramento, CA; Department of 
      Biochemistry and Molecular Medicine, University of California at Davis, 
      Sacramento, CA. Electronic address: paghosh@ucdavis.edu.
LA  - eng
GR  - I01 BX000400/BX/BLRD VA/United States
GR  - R01 CA133209/CA/NCI NIH HHS/United States
GR  - R01 CA185509/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20180504
PL  - United States
TA  - Neoplasia
JT  - Neoplasia (New York, N.Y.)
JID - 100886622
RN  - 0 (Eukaryotic Initiation Factor-4E)
RN  - 0 (RNA, Messenger)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Eukaryotic Initiation Factor-4E/*genetics
MH  - Humans
MH  - Male
MH  - Mitogen-Activated Protein Kinases/genetics
MH  - Phosphorylation/*genetics
MH  - Prostatic Neoplasms/*genetics
MH  - RNA, Messenger/genetics
MH  - Signal Transduction/genetics
PMC - PMC5994774
EDAT- 2018/05/08 06:00
MHDA- 2018/11/27 06:00
PMCR- 2018/05/04
CRDT- 2018/05/07 06:00
PHST- 2018/01/18 00:00 [received]
PHST- 2018/04/09 00:00 [revised]
PHST- 2018/04/10 00:00 [accepted]
PHST- 2018/05/08 06:00 [pubmed]
PHST- 2018/11/27 06:00 [medline]
PHST- 2018/05/07 06:00 [entrez]
PHST- 2018/05/04 00:00 [pmc-release]
AID - S1476-5586(18)30001-0 [pii]
AID - 10.1016/j.neo.2018.04.003 [doi]
PST - ppublish
SO  - Neoplasia. 2018 Jun;20(6):563-573. doi: 10.1016/j.neo.2018.04.003. Epub 2018 May 
      4.