PMID- 38172654
OWN - NLM
STAT- MEDLINE
DCOM- 20240105
LR  - 20240106
IS  - 1689-1392 (Electronic)
IS  - 1425-8153 (Print)
IS  - 1425-8153 (Linking)
VI  - 29
IP  - 1
DP  - 2024 Jan 3
TI  - Oncogenic activation of EEF1A2 expression: a journey from a putative to an 
      established oncogene.
PG  - 6
LID - 10.1186/s11658-023-00519-9 [doi]
LID - 6
AB  - Protein synthesis via translation is a central process involving several 
      essential proteins called translation factors. Although traditionally described 
      as cellular "housekeepers," multiple studies have now supported that protein 
      initiation and elongation factors regulate cell growth, apoptosis, and 
      tumorigenesis. One such translation factor is eukaryotic elongation factor 1 
      alpha 2 (EEF1A2), a member of the eukaryotic elongation factor family, which has 
      a canonical role in the delivery of aminoacyl-tRNA to the A-site of the ribosome 
      in a guanosine 5'-triphosphate (GTP)-dependent manner. EEF1A2 differs from its 
      closely related isoform, EEF1A1, in tissue distribution. While EEF1A1 is present 
      ubiquitously, EEF1A2 replaces it in specialized tissues. The reason why certain 
      specialized tissues need to essentially switch EEF1A1 expression altogether with 
      EEF1A2 remains to be answered. Abnormal "switch on" of the EEF1A2 gene in normal 
      tissues is witnessed and is seen as a cause of oncogenic transformation in a wide 
      variety of solid tumors. This review presents the journey of finding increased 
      expression of EEF1A2 in multiple cancers, establishing molecular mechanism, and 
      exploring it as a target for cancer therapy. More precisely, we have compiled 
      studies in seven types of cancers that have reported EEF1A2 overexpression. We 
      have discussed the effect of aberrant EEF1A2 expression on the oncogenic 
      properties of cells, signaling pathways, and interacting partners of EEF1A2. More 
      importantly, in the last part, we have discussed the unique potential of EEF1A2 
      as a therapeutic target. This review article gives an up-to-date account of 
      EEF1A2 as an oncogene and can draw the attention of the scientific community, 
      attracting more research.
CI  - (c) 2023. The Author(s).
FAU - Patel, Saket Awadhesbhai
AU  - Patel SA
AD  - School of Biological Sciences, National Institute of Science Education and 
      Research, Room No. 204, P.O. Jatni, Khurda, Bhubaneswar, Odisha, 752050, India.
AD  - Homi Bhabha National Institute, Training School Complex, Anushaktinagar, Mumbai, 
      400094, India.
FAU - Hassan, Md Khurshidul
AU  - Hassan MK
AD  - School of Biological Sciences, National Institute of Science Education and 
      Research, Room No. 204, P.O. Jatni, Khurda, Bhubaneswar, Odisha, 752050, India.
AD  - Homi Bhabha National Institute, Training School Complex, Anushaktinagar, Mumbai, 
      400094, India.
FAU - Dixit, Manjusha
AU  - Dixit M
AUID- ORCID: 0000-0002-6997-1054
AD  - School of Biological Sciences, National Institute of Science Education and 
      Research, Room No. 204, P.O. Jatni, Khurda, Bhubaneswar, Odisha, 752050, India. 
      manjusha@niser.ac.in.
AD  - Homi Bhabha National Institute, Training School Complex, Anushaktinagar, Mumbai, 
      400094, India. manjusha@niser.ac.in.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20240103
PL  - England
TA  - Cell Mol Biol Lett
JT  - Cellular & molecular biology letters
JID - 9607427
RN  - 0 (Peptide Elongation Factor 1)
RN  - 0 (Protein Isoforms)
RN  - 0 (EEF1A2 protein, human)
SB  - IM
MH  - Humans
MH  - *Peptide Elongation Factor 1/genetics/metabolism
MH  - Oncogenes
MH  - Protein Isoforms/genetics
MH  - Signal Transduction
MH  - *Neoplasms/genetics
PMC - PMC10765684
OTO - NOTNLM
OT  - AKT
OT  - Cancer
OT  - EEF1A1
OT  - EEF1A2
OT  - PI3K
COIS- The authors have no relevant financial or non-financial interest to disclose.
EDAT- 2024/01/04 11:43
MHDA- 2024/01/05 06:42
PMCR- 2024/01/03
CRDT- 2024/01/03 23:43
PHST- 2023/09/04 00:00 [received]
PHST- 2023/12/01 00:00 [accepted]
PHST- 2024/01/05 06:42 [medline]
PHST- 2024/01/04 11:43 [pubmed]
PHST- 2024/01/03 23:43 [entrez]
PHST- 2024/01/03 00:00 [pmc-release]
AID - 10.1186/s11658-023-00519-9 [pii]
AID - 519 [pii]
AID - 10.1186/s11658-023-00519-9 [doi]
PST - epublish
SO  - Cell Mol Biol Lett. 2024 Jan 3;29(1):6. doi: 10.1186/s11658-023-00519-9.