The Role of PI3K in Met Driven Cancer: A Recap
The Receptor Tyrosine Kinase (RTK) Met, overexpressed or mutated in cancer, plays a major role in cancer progression and represents an attractive target for cancer therapy. However RTK inhibitors can lead to drug resistance, explaining the necessity to develop therapies that target downstream signal...
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doaj-a3facb48bf1d407a865077f69bb323d32020-11-24T20:45:31ZengFrontiers Media S.A.Frontiers in Molecular Biosciences2296-889X2018-10-01510.3389/fmolb.2018.00086412727The Role of PI3K in Met Driven Cancer: A RecapAlexia Hervieu0Alexia Hervieu1Stéphanie Kermorgant2Signal Transduction and Molecular Pharmacology Team, Cancer Therapeutics Division, Institute of Cancer Research, Sutton, United KingdomSpatial Signalling Team, Centre for Tumor Biology, Barts Cancer Institute, Queen Mary University of London, London, United KingdomSpatial Signalling Team, Centre for Tumor Biology, Barts Cancer Institute, Queen Mary University of London, London, United KingdomThe Receptor Tyrosine Kinase (RTK) Met, overexpressed or mutated in cancer, plays a major role in cancer progression and represents an attractive target for cancer therapy. However RTK inhibitors can lead to drug resistance, explaining the necessity to develop therapies that target downstream signaling. Phosphatidylinositide 3-kinase (PI3K) is one of the most deregulated pathways in cancer and implicated in various types of cancer. PI3K signaling is also a major signaling pathway downstream of RTK, including Met. PI3K major effectors include Akt and “mechanistic Target of Rapamycin” (mTOR), which each play key roles in numerous and various cell functions. Advancements made due to the development of molecular and pharmaceutical tools now allow us to delve into the roles of each independently. In this review, we summarize the current understanding we possess of the activation and role of PI3K/Akt/mTOR, downstream of Met, in cancer.https://www.frontiersin.org/article/10.3389/fmolb.2018.00086/fullMetPI3KAktmTORcancersignaling |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Alexia Hervieu Alexia Hervieu Stéphanie Kermorgant |
spellingShingle |
Alexia Hervieu Alexia Hervieu Stéphanie Kermorgant The Role of PI3K in Met Driven Cancer: A Recap Frontiers in Molecular Biosciences Met PI3K Akt mTOR cancer signaling |
author_facet |
Alexia Hervieu Alexia Hervieu Stéphanie Kermorgant |
author_sort |
Alexia Hervieu |
title |
The Role of PI3K in Met Driven Cancer: A Recap |
title_short |
The Role of PI3K in Met Driven Cancer: A Recap |
title_full |
The Role of PI3K in Met Driven Cancer: A Recap |
title_fullStr |
The Role of PI3K in Met Driven Cancer: A Recap |
title_full_unstemmed |
The Role of PI3K in Met Driven Cancer: A Recap |
title_sort |
role of pi3k in met driven cancer: a recap |
publisher |
Frontiers Media S.A. |
series |
Frontiers in Molecular Biosciences |
issn |
2296-889X |
publishDate |
2018-10-01 |
description |
The Receptor Tyrosine Kinase (RTK) Met, overexpressed or mutated in cancer, plays a major role in cancer progression and represents an attractive target for cancer therapy. However RTK inhibitors can lead to drug resistance, explaining the necessity to develop therapies that target downstream signaling. Phosphatidylinositide 3-kinase (PI3K) is one of the most deregulated pathways in cancer and implicated in various types of cancer. PI3K signaling is also a major signaling pathway downstream of RTK, including Met. PI3K major effectors include Akt and “mechanistic Target of Rapamycin” (mTOR), which each play key roles in numerous and various cell functions. Advancements made due to the development of molecular and pharmaceutical tools now allow us to delve into the roles of each independently. In this review, we summarize the current understanding we possess of the activation and role of PI3K/Akt/mTOR, downstream of Met, in cancer. |
topic |
Met PI3K Akt mTOR cancer signaling |
url |
https://www.frontiersin.org/article/10.3389/fmolb.2018.00086/full |
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