Unresponsiveness of colon cancer to BRAF(V600E) inhibition through feedback activation of EGFR
Inhibition of activated BRAF has been ineffective in colon cancers with the mutation; here, this is shown to be due to the feedback activation of the epidermal growth factor receptor (EGFR) in response to BRAF inhibition. Inhibition of the BRAF(V600E) oncoprotein by the small-molecule drug PLX4032 (...
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| Vydáno v: | Nature (London) Ročník 483; číslo 7387; s. 100 - 103 |
|---|---|
| Hlavní autoři: | , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
| Vydáno: |
London
Nature Publishing Group UK
01.03.2012
Nature Publishing Group |
| Témata: | |
| ISSN: | 0028-0836, 1476-4687, 1476-4687 |
| On-line přístup: | Získat plný text |
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| Abstract | Inhibition of activated BRAF has been ineffective in colon cancers with the mutation; here, this is shown to be due to the feedback activation of the epidermal growth factor receptor (EGFR) in response to BRAF inhibition.
Inhibition of the BRAF(V600E) oncoprotein by the small-molecule drug PLX4032 (vemurafenib) is highly effective in the treatment of melanoma
1
. However, colon cancer patients harbouring the same
BRAF
(
V600E
) oncogenic lesion have poor prognosis and show only a very limited response to this drug
2
,
3
,
4
. To investigate the cause of the limited therapeutic effect of PLX4032 in
BRAF
(
V600E
) mutant colon tumours, here we performed an RNA-interference-based genetic screen in human cells to search for kinases whose knockdown synergizes with BRAF(V600E) inhibition. We report that blockade of the epidermal growth factor receptor (EGFR) shows strong synergy with BRAF(V600E) inhibition. We find in multiple
BRAF
(
V600E
) mutant colon cancers that inhibition of EGFR by the antibody drug cetuximab or the small-molecule drugs gefitinib or erlotinib is strongly synergistic with BRAF(V600E) inhibition, both
in vitro
and
in vivo
. Mechanistically, we find that BRAF(V600E) inhibition causes a rapid feedback activation of EGFR, which supports continued proliferation in the presence of BRAF(V600E) inhibition. Melanoma cells express low levels of EGFR and are therefore not subject to this feedback activation. Consistent with this, we find that ectopic expression of
EGFR
in melanoma cells is sufficient to cause resistance to PLX4032. Our data suggest that
BRAF
(
V600E
) mutant colon cancers (approximately 8–10% of all colon cancers
2
,
3
,
5
), for which there are currently no targeted treatment options available, might benefit from combination therapy consisting of BRAF and EGFR inhibitors. |
|---|---|
| AbstractList | Inhibition of the BRAF(V600E) oncoprotein by the small-molecule drug PLX4032 (vemurafenib) is highly effective in the treatment of melanoma. However, colon cancer patients harbouring the same BRAF(V600E) oncogenic lesion have poor prognosis and show only a very limited response to this drug. To investigate the cause of the limited therapeutic effect of PLX4032 in BRAF(V600E) mutant colon tumours, here we performed an RNA-interference-based genetic screen in human cells to search for kinases whose knockdown synergizes with BRAF(V600E) inhibition. We report that blockade of the epidermal growth factor receptor (EGFR) shows strong synergy with BRAF(V600E) inhibition. We find in multiple BRAF(V600E) mutant colon cancers that inhibition of EGFR by the antibody drug cetuximab or the small-molecule drugs gefitinib or erlotinib is strongly synergistic with BRAF(V600E) inhibition, both in vitro and in vivo. Mechanistically, we find that BRAF(V600E) inhibition causes a rapid feedback activation of EGFR, which supports continued proliferation in the presence of BRAF(V600E) inhibition. Melanoma cells express low levels of EGFR and are therefore not subject to this feedback activation. Consistent with this, we find that ectopic expression of EGFR in melanoma cells is sufficient to cause resistance to PLX4032. Our data suggest that BRAF(V600E) mutant colon cancers (approximately 8-10% of all colon cancers), for which there are currently no targeted treatment options available, might benefit from combination therapy consisting of BRAF and EGFR inhibitors.Inhibition of the BRAF(V600E) oncoprotein by the small-molecule drug PLX4032 (vemurafenib) is highly effective in the treatment of melanoma. However, colon cancer patients harbouring the same BRAF(V600E) oncogenic lesion have poor prognosis and show only a very limited response to this drug. To investigate the cause of the limited therapeutic effect of PLX4032 in BRAF(V600E) mutant colon tumours, here we performed an RNA-interference-based genetic screen in human cells to search for kinases whose knockdown synergizes with BRAF(V600E) inhibition. We report that blockade of the epidermal growth factor receptor (EGFR) shows strong synergy with BRAF(V600E) inhibition. We find in multiple BRAF(V600E) mutant colon cancers that inhibition of EGFR by the antibody drug cetuximab or the small-molecule drugs gefitinib or erlotinib is strongly synergistic with BRAF(V600E) inhibition, both in vitro and in vivo. Mechanistically, we find that BRAF(V600E) inhibition causes a rapid feedback activation of EGFR, which supports continued proliferation in the presence of BRAF(V600E) inhibition. Melanoma cells express low levels of EGFR and are therefore not subject to this feedback activation. Consistent with this, we find that ectopic expression of EGFR in melanoma cells is sufficient to cause resistance to PLX4032. Our data suggest that BRAF(V600E) mutant colon cancers (approximately 8-10% of all colon cancers), for which there are currently no targeted treatment options available, might benefit from combination therapy consisting of BRAF and EGFR inhibitors. [...] Cdc25A can bind to and dephosphorylate EGFR16. [...] treatment of WiDr cells with PLX4032 inhibited phosphorylation ofCDC25C at Thr 48 (Fig. 2f), which has been shown to be required for its phosphatase activity15.\n At first glance, it would seem counterintuitive to consider treating a BRAF mutant colon cancer with an EGFR inhibitor, as multiple clinical studies in colon cancer have shown that EGFR inhibition is without clinical benefit when either KRAS or BRAF is mutated downstream of EGFR7,13,14. Inhibition of activated BRAF has been ineffective in colon cancers with the mutation; here, this is shown to be due to the feedback activation of the epidermal growth factor receptor (EGFR) in response to BRAF inhibition. Inhibition of the BRAF(V600E) oncoprotein by the small-molecule drug PLX4032 (vemurafenib) is highly effective in the treatment of melanoma 1 . However, colon cancer patients harbouring the same BRAF ( V600E ) oncogenic lesion have poor prognosis and show only a very limited response to this drug 2 , 3 , 4 . To investigate the cause of the limited therapeutic effect of PLX4032 in BRAF ( V600E ) mutant colon tumours, here we performed an RNA-interference-based genetic screen in human cells to search for kinases whose knockdown synergizes with BRAF(V600E) inhibition. We report that blockade of the epidermal growth factor receptor (EGFR) shows strong synergy with BRAF(V600E) inhibition. We find in multiple BRAF ( V600E ) mutant colon cancers that inhibition of EGFR by the antibody drug cetuximab or the small-molecule drugs gefitinib or erlotinib is strongly synergistic with BRAF(V600E) inhibition, both in vitro and in vivo . Mechanistically, we find that BRAF(V600E) inhibition causes a rapid feedback activation of EGFR, which supports continued proliferation in the presence of BRAF(V600E) inhibition. Melanoma cells express low levels of EGFR and are therefore not subject to this feedback activation. Consistent with this, we find that ectopic expression of EGFR in melanoma cells is sufficient to cause resistance to PLX4032. Our data suggest that BRAF ( V600E ) mutant colon cancers (approximately 8–10% of all colon cancers 2 , 3 , 5 ), for which there are currently no targeted treatment options available, might benefit from combination therapy consisting of BRAF and EGFR inhibitors. Inhibition of the BRAF(V600E) oncoprotein by the small-molecule drug PLX4032 (vemurafenib) is highly effective in the treatment of melanoma. However, colon cancer patients harbouring the same BRAF(V600E) oncogenic lesion have poor prognosis and show only a very limited response to this drug. To investigate the cause of the limited therapeutic effect of PLX4032 in BRAF(V600E) mutant colon tumours, here we performed an RNA-interference-based genetic screen in human cells to search for kinases whose knockdown synergizes with BRAF(V600E) inhibition. We report that blockade of the epidermal growth factor receptor (EGFR) shows strong synergy with BRAF(V600E) inhibition. We find in multiple BRAF(V600E) mutant colon cancers that inhibition of EGFR by the antibody drug cetuximab or the small-molecule drugs gefitinib or erlotinib is strongly synergistic with BRAF(V600E) inhibition, both in vitro and in vivo. Mechanistically, we find that BRAF(V600E) inhibition causes a rapid feedback activation of EGFR, which supports continued proliferation in the presence of BRAF(V600E) inhibition. Melanoma cells express low levels of EGFR and are therefore not subject to this feedback activation. Consistent with this, we find that ectopic expression of EGFR in melanoma cells is sufficient to cause resistance to PLX4032. Our data suggest that BRAF(V600E) mutant colon cancers (approximately 8-10% of all colon cancers), for which there are currently no targeted treatment options available, might benefit from combination therapy consisting of BRAF and EGFR inhibitors. |
| Author | Di Nicolantonio, Federica Bardelli, Alberto Zecchin, Davide Beijersbergen, Roderick L. Sun, Chong Huang, Sidong Salazar, Ramon Prahallad, Anirudh Bernards, René |
| Author_xml | – sequence: 1 givenname: Anirudh surname: Prahallad fullname: Prahallad, Anirudh organization: Division of Molecular Carcinogenesis, Center for Biomedical Genetics and Cancer Genomics Centre, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands – sequence: 2 givenname: Chong surname: Sun fullname: Sun, Chong organization: Division of Molecular Carcinogenesis, Center for Biomedical Genetics and Cancer Genomics Centre, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands – sequence: 3 givenname: Sidong surname: Huang fullname: Huang, Sidong organization: Division of Molecular Carcinogenesis, Center for Biomedical Genetics and Cancer Genomics Centre, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands – sequence: 4 givenname: Federica surname: Di Nicolantonio fullname: Di Nicolantonio, Federica organization: Laboratory of Molecular Genetics, Institute for Cancer Research and Treatment, University of Torino, Medical School, Str prov 142 Km 3.95, 10060 Candiolo, Torino, Italy, FIRC-IFOM Institute for Molecular Oncology, Via Adamello 16, 20100 Milan, Italy – sequence: 5 givenname: Ramon surname: Salazar fullname: Salazar, Ramon organization: IDIBELL, Institut Català d’Oncologia L’Hospitalet de Llobregat, Gran Via s/n, km 2, 7 08907 L’Hospitalet-Barcelona, Spain – sequence: 6 givenname: Davide surname: Zecchin fullname: Zecchin, Davide organization: Laboratory of Molecular Genetics, Institute for Cancer Research and Treatment, University of Torino, Medical School, Str prov 142 Km 3.95, 10060 Candiolo, Torino, Italy – sequence: 7 givenname: Roderick L. surname: Beijersbergen fullname: Beijersbergen, Roderick L. organization: Division of Molecular Carcinogenesis, Center for Biomedical Genetics and Cancer Genomics Centre, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands – sequence: 8 givenname: Alberto surname: Bardelli fullname: Bardelli, Alberto organization: Laboratory of Molecular Genetics, Institute for Cancer Research and Treatment, University of Torino, Medical School, Str prov 142 Km 3.95, 10060 Candiolo, Torino, Italy, FIRC-IFOM Institute for Molecular Oncology, Via Adamello 16, 20100 Milan, Italy – sequence: 9 givenname: René surname: Bernards fullname: Bernards, René email: r.bernards@nki.nl organization: Division of Molecular Carcinogenesis, Center for Biomedical Genetics and Cancer Genomics Centre, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=25539125$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/22281684$$D View this record in MEDLINE/PubMed |
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| Copyright | Springer Nature Limited 2012 2015 INIST-CNRS Copyright Nature Publishing Group Mar 1, 2012 |
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| Keywords | Antineoplastic agent Epidermal growth factor receptor BRAF Gene Colon cancer Cancerology Established cell line Genetics Intestinal disease Protooncogene Human Rodentia Enzyme inhibitor Malignant tumor In vitro Colonic disease In vivo Vertebrata Chemotherapy Mammalia Treatment Mouse Animal C-Onc gene Digestive diseases Cancer |
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| Snippet | Inhibition of activated BRAF has been ineffective in colon cancers with the mutation; here, this is shown to be due to the feedback activation of the epidermal... Inhibition of the BRAF(V600E) oncoprotein by the small-molecule drug PLX4032 (vemurafenib) is highly effective in the treatment of melanoma. However, colon... [...] Cdc25A can bind to and dephosphorylate EGFR16. [...] treatment of WiDr cells with PLX4032 inhibited phosphorylation ofCDC25C at Thr 48 (Fig. 2f), which... |
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| Title | Unresponsiveness of colon cancer to BRAF(V600E) inhibition through feedback activation of EGFR |
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