In vivo genome-wide CRISPR screen reveals breast cancer vulnerabilities and synergistic mTOR/Hippo targeted combination therapy

Triple negative breast cancer (TNBC) patients exhibit poor survival outcomes and lack effective targeted therapies. Using unbiased in vivo genome-wide CRISPR screening, we interrogated cancer vulnerabilities in TNBC and identified an interplay between oncogenic and tumor suppressor pathways. This st...

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Published inNature communications Vol. 12; no. 1; p. 3055
Main Authors Dai, Meiou, Yan, Gang, Wang, Ni, Daliah, Girija, Edick, Ashlin M., Poulet, Sophie, Boudreault, Julien, Ali, Suhad, Burgos, Sergio A., Lebrun, Jean-Jacques
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 24.05.2021
Nature Publishing Group
Nature Portfolio
Subjects
13/109
13/2
13/31
13/51
13/95
14/63
38/43
42/47
45/23
45/41
631/67/1347
64/60
692/4028/67/69
96/1
96/106
96/2
Apoptosis
Breast cancer
Combination therapy
CRISPR
Genomes
Humanities and Social Sciences
In vivo methods and tests
Medical innovations
multidisciplinary
Pharmacology
Science
Science (multidisciplinary)
TOR protein
Tumor suppressor genes
Tumorigenesis
Tumors
Xenografts
Xenotransplantation
Yes-associated protein
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Abstract Triple negative breast cancer (TNBC) patients exhibit poor survival outcomes and lack effective targeted therapies. Using unbiased in vivo genome-wide CRISPR screening, we interrogated cancer vulnerabilities in TNBC and identified an interplay between oncogenic and tumor suppressor pathways. This study reveals tumor regulatory functions for essential components of the mTOR and Hippo pathways in TNBC. Using in vitro drug matrix synergy models and in vivo patient-derived xenografts, we further establish the therapeutic relevance of our findings and show that pharmacological inhibition of mTORC1/2 and oncoprotein YAP efficiently reduces tumorigenesis in TNBC. At the molecular level, we find that while verteporfin-induced YAP inhibition leads to apoptosis, torin1-mediated mTORC1/2 inhibition promotes macropinocytosis. Torin1-induced macropinocytosis further facilitates verteporfin uptake, thereby greatly enhancing its pro-apoptotic effects in cancer cells. Overall, our study underscores the power and robustness of in vivo CRISPR genome-wide screens in identifying clinically relevant and innovative therapeutic modalities in cancer. Triple negative breast cancer (TNBC) lack effective therapies. Here, through an in vivo genome-wide CRISPR screen in TNBCs, the authors identify tumorigenic functions for components of the mTORC1/2 complex and of the YAP/Hippo pathway, and demonstrate that pharmacological inhibition of mTOR and YAP reduces tumour growth in vivo.
AbstractList Triple negative breast cancer (TNBC) patients exhibit poor survival outcomes and lack effective targeted therapies. Using unbiased in vivo genome-wide CRISPR screening, we interrogated cancer vulnerabilities in TNBC and identified an interplay between oncogenic and tumor suppressor pathways. This study reveals tumor regulatory functions for essential components of the mTOR and Hippo pathways in TNBC. Using in vitro drug matrix synergy models and in vivo patient-derived xenografts, we further establish the therapeutic relevance of our findings and show that pharmacological inhibition of mTORC1/2 and oncoprotein YAP efficiently reduces tumorigenesis in TNBC. At the molecular level, we find that while verteporfin-induced YAP inhibition leads to apoptosis, torin1-mediated mTORC1/2 inhibition promotes macropinocytosis. Torin1-induced macropinocytosis further facilitates verteporfin uptake, thereby greatly enhancing its pro-apoptotic effects in cancer cells. Overall, our study underscores the power and robustness of in vivo CRISPR genome-wide screens in identifying clinically relevant and innovative therapeutic modalities in cancer. Triple negative breast cancer (TNBC) lack effective therapies. Here, through an in vivo genome-wide CRISPR screen in TNBCs, the authors identify tumorigenic functions for components of the mTORC1/2 complex and of the YAP/Hippo pathway, and demonstrate that pharmacological inhibition of mTOR and YAP reduces tumour growth in vivo.
Abstract Triple negative breast cancer (TNBC) patients exhibit poor survival outcomes and lack effective targeted therapies. Using unbiased in vivo genome-wide CRISPR screening, we interrogated cancer vulnerabilities in TNBC and identified an interplay between oncogenic and tumor suppressor pathways. This study reveals tumor regulatory functions for essential components of the mTOR and Hippo pathways in TNBC. Using in vitro drug matrix synergy models and in vivo patient-derived xenografts, we further establish the therapeutic relevance of our findings and show that pharmacological inhibition of mTORC1/2 and oncoprotein YAP efficiently reduces tumorigenesis in TNBC. At the molecular level, we find that while verteporfin-induced YAP inhibition leads to apoptosis, torin1-mediated mTORC1/2 inhibition promotes macropinocytosis. Torin1-induced macropinocytosis further facilitates verteporfin uptake, thereby greatly enhancing its pro-apoptotic effects in cancer cells. Overall, our study underscores the power and robustness of in vivo CRISPR genome-wide screens in identifying clinically relevant and innovative therapeutic modalities in cancer.
Triple negative breast cancer (TNBC) lack effective therapies. Here, through an in vivo genome-wide CRISPR screen in TNBCs, the authors identify tumorigenic functions for components of the mTORC1/2 complex and of the YAP/Hippo pathway, and demonstrate that pharmacological inhibition of mTOR and YAP reduces tumour growth in vivo.
Triple negative breast cancer (TNBC) patients exhibit poor survival outcomes and lack effective targeted therapies. Using unbiased in vivo genome-wide CRISPR screening, we interrogated cancer vulnerabilities in TNBC and identified an interplay between oncogenic and tumor suppressor pathways. This study reveals tumor regulatory functions for essential components of the mTOR and Hippo pathways in TNBC. Using in vitro drug matrix synergy models and in vivo patient-derived xenografts, we further establish the therapeutic relevance of our findings and show that pharmacological inhibition of mTORC1/2 and oncoprotein YAP efficiently reduces tumorigenesis in TNBC. At the molecular level, we find that while verteporfin-induced YAP inhibition leads to apoptosis, torin1-mediated mTORC1/2 inhibition promotes macropinocytosis. Torin1-induced macropinocytosis further facilitates verteporfin uptake, thereby greatly enhancing its pro-apoptotic effects in cancer cells. Overall, our study underscores the power and robustness of in vivo CRISPR genome-wide screens in identifying clinically relevant and innovative therapeutic modalities in cancer.Triple negative breast cancer (TNBC) lack effective therapies. Here, through an in vivo genome-wide CRISPR screen in TNBCs, the authors identify tumorigenic functions for components of the mTORC1/2 complex and of the YAP/Hippo pathway, and demonstrate that pharmacological inhibition of mTOR and YAP reduces tumour growth in vivo.
ArticleNumber 3055
Author Boudreault, Julien
Dai, Meiou
Ali, Suhad
Wang, Ni
Daliah, Girija
Edick, Ashlin M.
Burgos, Sergio A.
Lebrun, Jean-Jacques
Poulet, Sophie
Yan, Gang
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SSID ssj0000391844
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Snippet Triple negative breast cancer (TNBC) patients exhibit poor survival outcomes and lack effective targeted therapies. Using unbiased in vivo genome-wide CRISPR...
Abstract Triple negative breast cancer (TNBC) patients exhibit poor survival outcomes and lack effective targeted therapies. Using unbiased in vivo genome-wide...
Triple negative breast cancer (TNBC) lack effective therapies. Here, through an in vivo genome-wide CRISPR screen in TNBCs, the authors identify tumorigenic...
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Apoptosis
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TOR protein
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Title In vivo genome-wide CRISPR screen reveals breast cancer vulnerabilities and synergistic mTOR/Hippo targeted combination therapy
URI https://link.springer.com/article/10.1038/s41467-021-23316-4
https://www.proquest.com/docview/2531420584
https://search.proquest.com/docview/2532244505
https://pubmed.ncbi.nlm.nih.gov/PMC8144221
https://doaj.org/article/38501aae84394eee911b035fc5797ebd
Volume 12
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