Abstract
An increasing amount of evidence has shown that tumor suppressors can become oncogenes, or vice versa, but the mechanism behind this is unclear. Recent findings have suggested that phosphatase and tensin homolog (PTEN) is one of the powerful switches for the conversion between tumor suppressors and oncogenes. PTEN regulates a number of cellular processes, including cell death and proliferation, through the phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) pathway. Furthermore, a number of studies have suggested that PTEN deletions may alter various functions of certain tumor suppressor and oncogenic proteins. The aim of the present review was to analyze specific cases driven by PTEN loss/AKT activation, including aberrant signaling pathways and novel drug targets for clinical application in personalized medicine. The findings illustrate how PTEN loss and/or AKT activation switches MDM2-dependent p53 downregulation, and induces conversion between oncogene and tumor suppressor in enhancer of zeste homolog 2, BTB domain-containing 7A, alternative reading frame 2, p27 and breast cancer 1, early onset, through multiple mechanisms. This review highlights the genetic basis of complex drug targets and provides insights into the rationale of precision cancer therapy.
| Original language | English |
|---|---|
| Pages (from-to) | 375-378 |
| Number of pages | 4 |
| Journal | Oncology Letters |
| Volume | 12 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - Jul 1 2016 |
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Keywords
- Molecular switch
- Oncogene
- PTEN
- Tumor suppressor
ASJC Scopus subject areas
- Oncology
- Cancer Research
Cite this
Power of PTEN/AKT : Molecular switch between tumor suppressors and oncogenes. / Xie, Yingqiu; Naizabekov, Sanzhar; Chen, Zhanlin; Tokay, Tursonjan.
In: Oncology Letters, Vol. 12, No. 1, 01.07.2016, p. 375-378.Research output: Contribution to journal › Review article
}
TY - JOUR
T1 - Power of PTEN/AKT
T2 - Molecular switch between tumor suppressors and oncogenes
AU - Xie, Yingqiu
AU - Naizabekov, Sanzhar
AU - Chen, Zhanlin
AU - Tokay, Tursonjan
PY - 2016/7/1
Y1 - 2016/7/1
N2 - An increasing amount of evidence has shown that tumor suppressors can become oncogenes, or vice versa, but the mechanism behind this is unclear. Recent findings have suggested that phosphatase and tensin homolog (PTEN) is one of the powerful switches for the conversion between tumor suppressors and oncogenes. PTEN regulates a number of cellular processes, including cell death and proliferation, through the phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) pathway. Furthermore, a number of studies have suggested that PTEN deletions may alter various functions of certain tumor suppressor and oncogenic proteins. The aim of the present review was to analyze specific cases driven by PTEN loss/AKT activation, including aberrant signaling pathways and novel drug targets for clinical application in personalized medicine. The findings illustrate how PTEN loss and/or AKT activation switches MDM2-dependent p53 downregulation, and induces conversion between oncogene and tumor suppressor in enhancer of zeste homolog 2, BTB domain-containing 7A, alternative reading frame 2, p27 and breast cancer 1, early onset, through multiple mechanisms. This review highlights the genetic basis of complex drug targets and provides insights into the rationale of precision cancer therapy.
AB - An increasing amount of evidence has shown that tumor suppressors can become oncogenes, or vice versa, but the mechanism behind this is unclear. Recent findings have suggested that phosphatase and tensin homolog (PTEN) is one of the powerful switches for the conversion between tumor suppressors and oncogenes. PTEN regulates a number of cellular processes, including cell death and proliferation, through the phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) pathway. Furthermore, a number of studies have suggested that PTEN deletions may alter various functions of certain tumor suppressor and oncogenic proteins. The aim of the present review was to analyze specific cases driven by PTEN loss/AKT activation, including aberrant signaling pathways and novel drug targets for clinical application in personalized medicine. The findings illustrate how PTEN loss and/or AKT activation switches MDM2-dependent p53 downregulation, and induces conversion between oncogene and tumor suppressor in enhancer of zeste homolog 2, BTB domain-containing 7A, alternative reading frame 2, p27 and breast cancer 1, early onset, through multiple mechanisms. This review highlights the genetic basis of complex drug targets and provides insights into the rationale of precision cancer therapy.
KW - Molecular switch
KW - Oncogene
KW - PTEN
KW - Tumor suppressor
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UR - http://www.scopus.com/inward/citedby.url?scp=84973443327&partnerID=8YFLogxK
U2 - 10.3892/ol.2016.4636
DO - 10.3892/ol.2016.4636
M3 - Review article
AN - SCOPUS:84973443327
VL - 12
SP - 375
EP - 378
JO - Oncology Letters
JF - Oncology Letters
SN - 1792-1074
IS - 1
ER -