Abstract
The PI3K-AKT-mTOR signal transduction pathway regulates a variety of biological processes including cell growth, cell cycle progression and proliferation, cellular metabolism, and cytoskeleton reorganization. Fine-tuning of the phosphatidylinositol 3-kinase (PI3K) pathway signaling output is essential for the maintenance of tissue homeostasis and uncontrolled activation of this cascade leads to a number of human pathologies including cancer. Inactivation of the tumor suppressor phosphatase and tensin homologue deleted on Chromosome 10 (PTEN) and/or activating mutations in the proto-typical lipid kinase PI3K have emerged as some of the most frequent events associated with human cancer and as a result the PI3K pathway has become a highly sought-after target for cancer therapies. In this review we summarize the essential role of the PTEN-PI3K axis in controlling cellular behaviors by modulating activation of key proto-oncogenic molecular nodes and functional targets. Further, we highlight important functional redundancies and peculiarities of these two critical enzymes that over the last few decades have become a central part of the cancer research field and have instructed hundreds of pre-clinical and clinical trials to better cancer treatments.
| Original language | English |
|---|---|
| Article number | 153 |
| Number of pages | 11 |
| Journal | Biomolecules |
| Volume | 9 |
| Issue number | 4 |
| DOIs | |
| Publication status | Published - 17 Apr 2019 |
Keywords
- cancer predisposition syndromes
- mouse models of human cancer
- PI3K
- PTEN
- targeted therapies
Cite this
}
The PTEN⁻PI3K Axis in Cancer. / Papa, Antonella; Pandolfi, Pier Paolo.
In: Biomolecules, Vol. 9, No. 4, 153, 17.04.2019.Research output: Contribution to journal › Review Article › Research › peer-review
TY - JOUR
T1 - The PTEN⁻PI3K Axis in Cancer
AU - Papa, Antonella
AU - Pandolfi, Pier Paolo
PY - 2019/4/17
Y1 - 2019/4/17
N2 - The PI3K-AKT-mTOR signal transduction pathway regulates a variety of biological processes including cell growth, cell cycle progression and proliferation, cellular metabolism, and cytoskeleton reorganization. Fine-tuning of the phosphatidylinositol 3-kinase (PI3K) pathway signaling output is essential for the maintenance of tissue homeostasis and uncontrolled activation of this cascade leads to a number of human pathologies including cancer. Inactivation of the tumor suppressor phosphatase and tensin homologue deleted on Chromosome 10 (PTEN) and/or activating mutations in the proto-typical lipid kinase PI3K have emerged as some of the most frequent events associated with human cancer and as a result the PI3K pathway has become a highly sought-after target for cancer therapies. In this review we summarize the essential role of the PTEN-PI3K axis in controlling cellular behaviors by modulating activation of key proto-oncogenic molecular nodes and functional targets. Further, we highlight important functional redundancies and peculiarities of these two critical enzymes that over the last few decades have become a central part of the cancer research field and have instructed hundreds of pre-clinical and clinical trials to better cancer treatments.
AB - The PI3K-AKT-mTOR signal transduction pathway regulates a variety of biological processes including cell growth, cell cycle progression and proliferation, cellular metabolism, and cytoskeleton reorganization. Fine-tuning of the phosphatidylinositol 3-kinase (PI3K) pathway signaling output is essential for the maintenance of tissue homeostasis and uncontrolled activation of this cascade leads to a number of human pathologies including cancer. Inactivation of the tumor suppressor phosphatase and tensin homologue deleted on Chromosome 10 (PTEN) and/or activating mutations in the proto-typical lipid kinase PI3K have emerged as some of the most frequent events associated with human cancer and as a result the PI3K pathway has become a highly sought-after target for cancer therapies. In this review we summarize the essential role of the PTEN-PI3K axis in controlling cellular behaviors by modulating activation of key proto-oncogenic molecular nodes and functional targets. Further, we highlight important functional redundancies and peculiarities of these two critical enzymes that over the last few decades have become a central part of the cancer research field and have instructed hundreds of pre-clinical and clinical trials to better cancer treatments.
KW - cancer predisposition syndromes
KW - mouse models of human cancer
KW - PI3K
KW - PTEN
KW - targeted therapies
UR - http://www.scopus.com/inward/record.url?scp=85065015083&partnerID=8YFLogxK
U2 - 10.3390/biom9040153
DO - 10.3390/biom9040153
M3 - Review Article
VL - 9
JO - Biomolecules
JF - Biomolecules
SN - 2218-273X
IS - 4
M1 - 153
ER -