YAP/TAZ: Drivers of Tumor Growth, Metastasis, and Resistance to Therapy

The transcriptional co‐activators YAP (or YAP1) and TAZ (or WWTR1) are frequently activated during the growth and progression of many solid tumors, including lung, colorectal, breast, pancreatic, and liver carcinomas as well as melanoma and glioma. YAP/TAZ bind to TEAD‐family co‐activators to drive...

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Veröffentlicht in:BioEssays Jg. 42; H. 5; S. e1900162 - n/a
1. Verfasser: Thompson, Barry J.
Format: Journal Article
Sprache:Englisch
Veröffentlicht: United States Wiley Subscription Services, Inc 01.05.2020
Schlagworte:
1-Phosphatidylinositol 3-kinase
Activation
AKT protein
Brain tumors
Breast
Breast carcinoma
breasts
Cancer
cancer therapy
Cell migration
Cell survival
cell viability
Chemotherapy
drug therapy
Fibroblasts
G protein-coupled receptors
Glioma
Growth factors
Hippo pathway
Immunotherapy
Invasiveness
liver
lungs
Melanoma
Metastases
Metastasis
neoplasm cells
Pancreas
Pancreatic carcinoma
Radiation therapy
radiotherapy
Solid tumors
Stiffening
tissue growth
transcription (genetics)
Transcription factors
Tumors
Upstream
YAP/TAZ
Yes-associated protein
cancer
tissue growth
Hippo pathway
YAP/TAZ
ISSN:0265-9247, 1521-1878, 1521-1878
Online-Zugang:Volltext
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Abstract The transcriptional co‐activators YAP (or YAP1) and TAZ (or WWTR1) are frequently activated during the growth and progression of many solid tumors, including lung, colorectal, breast, pancreatic, and liver carcinomas as well as melanoma and glioma. YAP/TAZ bind to TEAD‐family co‐activators to drive cancer cell survival, proliferation, invasive migration, and metastasis. YAP/TAZ activation may also confer resistance to chemotherapy, radiotherapy, or immunotherapy. YAP‐TEAD cooperates with the RAS‐induced AP‐1 (FOS/JUN) transcription factor to drive tumor growth and cooperates with MRTF‐SRF to promote activation of cancer‐associated fibroblasts, matrix stiffening, and metastasis. The key upstream repressor of YAP/TAZ activation is the Hippo (MST1/2‐LATS1/2) pathway and the key upstream activators are mechanically induced Integrin‐SRC and E‐cadherin‐AJUBA/TRIP6/LIMD1, growth factor induced PI3K‐AKT, and inflammation‐induced G‐protein coupled receptor (GPCR) signals, all of which antagonize the Hippo pathway. In this review, strategies to target YAP/TAZ activity in cancer are discussed along with the prospects for synergy with established pillars of cancer therapy. YAP and TAZ are key mediators of wound healing and tissue regeneration responses as well as important drivers of solid tumor growth, metastasis, and resistance to therapy, making them attractive therapeutic targets for cancer.
AbstractList The transcriptional co‐activators YAP (or YAP1) and TAZ (or WWTR1) are frequently activated during the growth and progression of many solid tumors, including lung, colorectal, breast, pancreatic, and liver carcinomas as well as melanoma and glioma. YAP/TAZ bind to TEAD‐family co‐activators to drive cancer cell survival, proliferation, invasive migration, and metastasis. YAP/TAZ activation may also confer resistance to chemotherapy, radiotherapy, or immunotherapy. YAP‐TEAD cooperates with the RAS‐induced AP‐1 (FOS/JUN) transcription factor to drive tumor growth and cooperates with MRTF‐SRF to promote activation of cancer‐associated fibroblasts, matrix stiffening, and metastasis. The key upstream repressor of YAP/TAZ activation is the Hippo (MST1/2‐LATS1/2) pathway and the key upstream activators are mechanically induced Integrin‐SRC and E‐cadherin‐AJUBA/TRIP6/LIMD1, growth factor induced PI3K‐AKT, and inflammation‐induced G‐protein coupled receptor (GPCR) signals, all of which antagonize the Hippo pathway. In this review, strategies to target YAP/TAZ activity in cancer are discussed along with the prospects for synergy with established pillars of cancer therapy.
The transcriptional co-activators YAP (or YAP1) and TAZ (or WWTR1) are frequently activated during the growth and progression of many solid tumors, including lung, colorectal, breast, pancreatic, and liver carcinomas as well as melanoma and glioma. YAP/TAZ bind to TEAD-family co-activators to drive cancer cell survival, proliferation, invasive migration, and metastasis. YAP/TAZ activation may also confer resistance to chemotherapy, radiotherapy, or immunotherapy. YAP-TEAD cooperates with the RAS-induced AP-1 (FOS/JUN) transcription factor to drive tumor growth and cooperates with MRTF-SRF to promote activation of cancer-associated fibroblasts, matrix stiffening, and metastasis. The key upstream repressor of YAP/TAZ activation is the Hippo (MST1/2-LATS1/2) pathway and the key upstream activators are mechanically induced Integrin-SRC and E-cadherin-AJUBA/TRIP6/LIMD1, growth factor induced PI3K-AKT, and inflammation-induced G-protein coupled receptor (GPCR) signals, all of which antagonize the Hippo pathway. In this review, strategies to target YAP/TAZ activity in cancer are discussed along with the prospects for synergy with established pillars of cancer therapy.The transcriptional co-activators YAP (or YAP1) and TAZ (or WWTR1) are frequently activated during the growth and progression of many solid tumors, including lung, colorectal, breast, pancreatic, and liver carcinomas as well as melanoma and glioma. YAP/TAZ bind to TEAD-family co-activators to drive cancer cell survival, proliferation, invasive migration, and metastasis. YAP/TAZ activation may also confer resistance to chemotherapy, radiotherapy, or immunotherapy. YAP-TEAD cooperates with the RAS-induced AP-1 (FOS/JUN) transcription factor to drive tumor growth and cooperates with MRTF-SRF to promote activation of cancer-associated fibroblasts, matrix stiffening, and metastasis. The key upstream repressor of YAP/TAZ activation is the Hippo (MST1/2-LATS1/2) pathway and the key upstream activators are mechanically induced Integrin-SRC and E-cadherin-AJUBA/TRIP6/LIMD1, growth factor induced PI3K-AKT, and inflammation-induced G-protein coupled receptor (GPCR) signals, all of which antagonize the Hippo pathway. In this review, strategies to target YAP/TAZ activity in cancer are discussed along with the prospects for synergy with established pillars of cancer therapy.
The transcriptional co‐activators YAP (or YAP1) and TAZ (or WWTR1) are frequently activated during the growth and progression of many solid tumors, including lung, colorectal, breast, pancreatic, and liver carcinomas as well as melanoma and glioma. YAP/TAZ bind to TEAD‐family co‐activators to drive cancer cell survival, proliferation, invasive migration, and metastasis. YAP/TAZ activation may also confer resistance to chemotherapy, radiotherapy, or immunotherapy. YAP‐TEAD cooperates with the RAS‐induced AP‐1 (FOS/JUN) transcription factor to drive tumor growth and cooperates with MRTF‐SRF to promote activation of cancer‐associated fibroblasts, matrix stiffening, and metastasis. The key upstream repressor of YAP/TAZ activation is the Hippo (MST1/2‐LATS1/2) pathway and the key upstream activators are mechanically induced Integrin‐SRC and E‐cadherin‐AJUBA/TRIP6/LIMD1, growth factor induced PI3K‐AKT, and inflammation‐induced G‐protein coupled receptor (GPCR) signals, all of which antagonize the Hippo pathway. In this review, strategies to target YAP/TAZ activity in cancer are discussed along with the prospects for synergy with established pillars of cancer therapy. YAP and TAZ are key mediators of wound healing and tissue regeneration responses as well as important drivers of solid tumor growth, metastasis, and resistance to therapy, making them attractive therapeutic targets for cancer.
Author Thompson, Barry J.
Author_xml – sequence: 1
  givenname: Barry J.
  orcidid: 0000-0002-0103-040X
  surname: Thompson
  fullname: Thompson, Barry J.
  email: Barry.Thompson@anu.edu.au
  organization: The Australian National University
BackLink https://www.ncbi.nlm.nih.gov/pubmed/32128850$$D View this record in MEDLINE/PubMed
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Snippet The transcriptional co‐activators YAP (or YAP1) and TAZ (or WWTR1) are frequently activated during the growth and progression of many solid tumors, including...
The transcriptional co-activators YAP (or YAP1) and TAZ (or WWTR1) are frequently activated during the growth and progression of many solid tumors, including...
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SubjectTerms 1-Phosphatidylinositol 3-kinase
Activation
AKT protein
Brain tumors
Breast
Breast carcinoma
breasts
Cancer
cancer therapy
Cell migration
Cell survival
cell viability
Chemotherapy
drug therapy
Fibroblasts
G protein-coupled receptors
Glioma
Growth factors
Hippo pathway
Immunotherapy
Invasiveness
liver
lungs
Melanoma
Metastases
Metastasis
neoplasm cells
Pancreas
Pancreatic carcinoma
Radiation therapy
radiotherapy
Solid tumors
Stiffening
tissue growth
transcription (genetics)
Transcription factors
Tumors
Upstream
YAP/TAZ
Yes-associated protein
Title YAP/TAZ: Drivers of Tumor Growth, Metastasis, and Resistance to Therapy
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fbies.201900162
https://www.ncbi.nlm.nih.gov/pubmed/32128850
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https://www.proquest.com/docview/2371143985
https://www.proquest.com/docview/2524217375
Volume 42
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