The role of RICTOR downstream of receptor tyrosine kinase in cancers

The importance of the network defined by phosphatidylinositol-3-kinase (PI3K), AKT and mammalian target of rapamycin (mTOR) downstream of Receptor Tyrosine Kinase (RTK) has been known for many years but the central role of RICTOR (rapamycin-insensitive companion of mTOR) in this pathway is only star...

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Bibliographic Details
Published in:Molecular cancer 2018-02, Vol.17 (1), p.39-39, Article 39
Main Authors: Jebali, Ahlem, Dumaz, Nicolas
Format: Article
Language:English
Subjects:
Analysis
Animals
Antineoplastic Agents - therapeutic use
Cancer
Development and progression
EGFR
HER2
Humans
Life Sciences
mTOR
mTOR inhibitors
mTORC2
Neoplasms - drug therapy
Neoplasms - genetics
Neoplasms - metabolism
PDGFR
Rapamycin-Insensitive Companion of mTOR Protein - genetics
Rapamycin-Insensitive Companion of mTOR Protein - metabolism
Receptor Protein-Tyrosine Kinases - genetics
Receptor Protein-Tyrosine Kinases - metabolism
Review
Signal Transduction - drug effects
Signal Transduction - genetics
TOR Serine-Threonine Kinases - genetics
TOR Serine-Threonine Kinases - metabolism
Tyrosine
Vascular endothelial growth factor
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Summary:The importance of the network defined by phosphatidylinositol-3-kinase (PI3K), AKT and mammalian target of rapamycin (mTOR) downstream of Receptor Tyrosine Kinase (RTK) has been known for many years but the central role of RICTOR (rapamycin-insensitive companion of mTOR) in this pathway is only starting to emerge. RICTOR is critical for mTORC2 (the mammalian target of rapamycin complex 2) kinase activity and as such plays a key role downstream of RTK. Alterations of RICTOR have been identified in a number of cancer cell types and its involvement in tumorigenesis has begun to be unraveled recently. Here, we summarize new research into the biology of RICTOR signaling in cancers focusing on tumors with altered RTK. We show that, as a key signaling node and critical effector of RTKs, RICTOR is becoming a valuable therapeutic target in cancer with altered RTK.
ISSN:1476-4598
1476-4598
DOI:10.1186/s12943-018-0794-0