Fatty acid synthase mediates EGFR palmitoylation in EGFR mutated non‐small cell lung cancer

Abstract Metabolic reprogramming is widely known as a hallmark of cancer cells to allow adaptation of cells to sustain survival signals. In this report, we describe a novel oncogenic signaling pathway exclusively acting in mutated epidermal growth factor receptor (EGFR) non‐small cell lung cancer (N...

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Main Authors: Azhar Ali, Elena Levantini, Jun Ting Teo, Julian Goggi, John G Clohessy, Chan Shuo Wu, Leilei Chen, Henry Yang, Indira Krishnan, Olivier Kocher, Junyan Zhang, Ross A Soo, Kishore Bhakoo, Tan Min Chin, Daniel G Tenen
Format: Article
Language:English
Published: Springer Nature 2018-02-01
Series:EMBO Molecular Medicine
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Online Access:https://doi.org/10.15252/emmm.201708313
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author Azhar Ali
Elena Levantini
Jun Ting Teo
Julian Goggi
John G Clohessy
Chan Shuo Wu
Leilei Chen
Henry Yang
Indira Krishnan
Olivier Kocher
Junyan Zhang
Ross A Soo
Kishore Bhakoo
Tan Min Chin
Daniel G Tenen
author_facet Azhar Ali
Elena Levantini
Jun Ting Teo
Julian Goggi
John G Clohessy
Chan Shuo Wu
Leilei Chen
Henry Yang
Indira Krishnan
Olivier Kocher
Junyan Zhang
Ross A Soo
Kishore Bhakoo
Tan Min Chin
Daniel G Tenen
author_sort Azhar Ali
collection DOAJ
description Abstract Metabolic reprogramming is widely known as a hallmark of cancer cells to allow adaptation of cells to sustain survival signals. In this report, we describe a novel oncogenic signaling pathway exclusively acting in mutated epidermal growth factor receptor (EGFR) non‐small cell lung cancer (NSCLC) with acquired tyrosine kinase inhibitor (TKI) resistance. Mutated EGFR mediates TKI resistance through regulation of the fatty acid synthase (FASN), which produces 16‐C saturated fatty acid palmitate. Our work shows that the persistent signaling by mutated EGFR in TKI‐resistant tumor cells relies on EGFR palmitoylation and can be targeted by Orlistat, an FDA‐approved anti‐obesity drug. Inhibition of FASN with Orlistat induces EGFR ubiquitination and abrogates EGFR mutant signaling, and reduces tumor growths both in culture systems and in vivo. Together, our data provide compelling evidence on the functional interrelationship between mutated EGFR and FASN and that the fatty acid metabolism pathway is a candidate target for acquired TKI‐resistant EGFR mutant NSCLC patients.
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institution Kabale University
issn 1757-4676
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language English
publishDate 2018-02-01
publisher Springer Nature
record_format Article
series EMBO Molecular Medicine
spelling doaj-art-01c6764a906741acac6682d904e68f0a2025-08-20T03:42:56ZengSpringer NatureEMBO Molecular Medicine1757-46761757-46842018-02-0110311910.15252/emmm.201708313Fatty acid synthase mediates EGFR palmitoylation in EGFR mutated non‐small cell lung cancerAzhar Ali0Elena Levantini1Jun Ting Teo2Julian Goggi3John G Clohessy4Chan Shuo Wu5Leilei Chen6Henry Yang7Indira Krishnan8Olivier Kocher9Junyan Zhang10Ross A Soo11Kishore Bhakoo12Tan Min Chin13Daniel G Tenen14Cancer Science Institute of Singapore, National University of SingaporeHarvard Stem Cell Institute, Harvard Medical SchoolCancer Science Institute of Singapore, National University of SingaporeSingapore Bioimaging Consortium (A*STAR)Beth Israel Deaconess Medical CenterCancer Science Institute of Singapore, National University of SingaporeCancer Science Institute of Singapore, National University of SingaporeCancer Science Institute of Singapore, National University of SingaporeBeth Israel Deaconess Medical CenterBeth Israel Deaconess Medical CenterBeth Israel Deaconess Medical CenterCancer Science Institute of Singapore, National University of SingaporeSingapore Bioimaging Consortium (A*STAR)Cancer Science Institute of Singapore, National University of SingaporeCancer Science Institute of Singapore, National University of SingaporeAbstract Metabolic reprogramming is widely known as a hallmark of cancer cells to allow adaptation of cells to sustain survival signals. In this report, we describe a novel oncogenic signaling pathway exclusively acting in mutated epidermal growth factor receptor (EGFR) non‐small cell lung cancer (NSCLC) with acquired tyrosine kinase inhibitor (TKI) resistance. Mutated EGFR mediates TKI resistance through regulation of the fatty acid synthase (FASN), which produces 16‐C saturated fatty acid palmitate. Our work shows that the persistent signaling by mutated EGFR in TKI‐resistant tumor cells relies on EGFR palmitoylation and can be targeted by Orlistat, an FDA‐approved anti‐obesity drug. Inhibition of FASN with Orlistat induces EGFR ubiquitination and abrogates EGFR mutant signaling, and reduces tumor growths both in culture systems and in vivo. Together, our data provide compelling evidence on the functional interrelationship between mutated EGFR and FASN and that the fatty acid metabolism pathway is a candidate target for acquired TKI‐resistant EGFR mutant NSCLC patients.https://doi.org/10.15252/emmm.201708313acquired resistanceEGFR‐TKIFASNNSCLCpalmitoylation
spellingShingle Azhar Ali
Elena Levantini
Jun Ting Teo
Julian Goggi
John G Clohessy
Chan Shuo Wu
Leilei Chen
Henry Yang
Indira Krishnan
Olivier Kocher
Junyan Zhang
Ross A Soo
Kishore Bhakoo
Tan Min Chin
Daniel G Tenen
Fatty acid synthase mediates EGFR palmitoylation in EGFR mutated non‐small cell lung cancer
EMBO Molecular Medicine
acquired resistance
EGFR‐TKI
FASN
NSCLC
palmitoylation
title Fatty acid synthase mediates EGFR palmitoylation in EGFR mutated non‐small cell lung cancer
title_full Fatty acid synthase mediates EGFR palmitoylation in EGFR mutated non‐small cell lung cancer
title_fullStr Fatty acid synthase mediates EGFR palmitoylation in EGFR mutated non‐small cell lung cancer
title_full_unstemmed Fatty acid synthase mediates EGFR palmitoylation in EGFR mutated non‐small cell lung cancer
title_short Fatty acid synthase mediates EGFR palmitoylation in EGFR mutated non‐small cell lung cancer
title_sort fatty acid synthase mediates egfr palmitoylation in egfr mutated non small cell lung cancer
topic acquired resistance
EGFR‐TKI
FASN
NSCLC
palmitoylation
url https://doi.org/10.15252/emmm.201708313
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