PTPN11 Is a Central Node in Intrinsic and Acquired Resistance to Targeted Cancer Drugs
Most BRAF (V600E) mutant melanomas are sensitive to selective BRAF inhibitors, but BRAF mutant colon cancers are intrinsically resistant to these drugs because of feedback activation of EGFR. We performed an RNA-interference-based genetic screen in BRAF mutant colon cancer cells to search for phosph...
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| Published in: | Cell reports (Cambridge) Vol. 12; no. 12; pp. 1978 - 1985 |
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| Main Authors: | , , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
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Elsevier Inc
29.09.2015
Elsevier |
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| ISSN: | 2211-1247, 2211-1247 |
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| Abstract | Most BRAF (V600E) mutant melanomas are sensitive to selective BRAF inhibitors, but BRAF mutant colon cancers are intrinsically resistant to these drugs because of feedback activation of EGFR. We performed an RNA-interference-based genetic screen in BRAF mutant colon cancer cells to search for phosphatases whose knockdown induces sensitivity to BRAF inhibition. We found that suppression of protein tyrosine phosphatase non-receptor type 11 (PTPN11) confers sensitivity to BRAF inhibitors in colon cancer. Mechanistically, we found that inhibition of PTPN11 blocks signaling from receptor tyrosine kinases (RTKs) to the RAS-MEK-ERK pathway. PTPN11 suppression is lethal to cells that are driven by activated RTKs and prevents acquired resistance to targeted cancer drugs that results from RTK activation. Our findings identify PTPN11 as a drug target to combat both intrinsic and acquired resistance to several targeted cancer drugs. Moreover, activated PTPN11 can serve as a biomarker of drug resistance resulting from RTK activation.
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•PTPN11 inhibition is synthetic lethal with BRAF inhibitors in BRAF mutant colon cancer•PTPN11 inhibition blocks the effects of EGFR activation by BRAF inhibitors•PTPN11 inhibition is lethal to cancers with activated RTKs•Phosphorylation of PTPN11 is a biomarker of RTK-driven drug resistance in melanoma
Using a synthetic lethality screen, Prahallad et al. report that PTPN11 suppression enhances the response to BRAF inhibition in BRAF mutant colon cancers by preventing the effects of receptor tyrosine kinase reactivation. These findings identify PTPN11 as a drug target to combat both intrinsic and acquired resistance to targeted cancer drugs. |
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| AbstractList | Most BRAF (V600E) mutant melanomas are sensitive to selective BRAF inhibitors, but BRAF mutant colon cancers are intrinsically resistant to these drugs because of feedback activation of EGFR. We performed an RNA-interference-based genetic screen in BRAF mutant colon cancer cells to search for phosphatases whose knockdown induces sensitivity to BRAF inhibition. We found that suppression of protein tyrosine phosphatase non-receptor type 11 (PTPN11) confers sensitivity to BRAF inhibitors in colon cancer. Mechanistically, we found that inhibition of PTPN11 blocks signaling from receptor tyrosine kinases (RTKs) to the RAS-MEK-ERK pathway. PTPN11 suppression is lethal to cells that are driven by activated RTKs and prevents acquired resistance to targeted cancer drugs that results from RTK activation. Our findings identify PTPN11 as a drug target to combat both intrinsic and acquired resistance to several targeted cancer drugs. Moreover, activated PTPN11 can serve as a biomarker of drug resistance resulting from RTK activation. Most BRAF (V600E) mutant melanomas are sensitive to selective BRAF inhibitors, but BRAF mutant colon cancers are intrinsically resistant to these drugs because of feedback activation of EGFR. We performed an RNA-interference-based genetic screen in BRAF mutant colon cancer cells to search for phosphatases whose knockdown induces sensitivity to BRAF inhibition. We found that suppression of protein tyrosine phosphatase non-receptor type 11 (PTPN11) confers sensitivity to BRAF inhibitors in colon cancer. Mechanistically, we found that inhibition of PTPN11 blocks signaling from receptor tyrosine kinases (RTKs) to the RAS-MEK-ERK pathway. PTPN11 suppression is lethal to cells that are driven by activated RTKs and prevents acquired resistance to targeted cancer drugs that results from RTK activation. Our findings identify PTPN11 as a drug target to combat both intrinsic and acquired resistance to several targeted cancer drugs. Moreover, activated PTPN11 can serve as a biomarker of drug resistance resulting from RTK activation. Most BRAF (V600E) mutant melanomas are sensitive to selective BRAF inhibitors, but BRAF mutant colon cancers are intrinsically resistant to these drugs because of feedback activation of EGFR. We performed an RNA-interference-based genetic screen in BRAF mutant colon cancer cells to search for phosphatases whose knockdown induces sensitivity to BRAF inhibition. We found that suppression of protein tyrosine phosphatase non-receptor type 11 (PTPN11) confers sensitivity to BRAF inhibitors in colon cancer. Mechanistically, we found that inhibition of PTPN11 blocks signaling from receptor tyrosine kinases (RTKs) to the RAS-MEK-ERK pathway. PTPN11 suppression is lethal to cells that are driven by activated RTKs and prevents acquired resistance to targeted cancer drugs that results from RTK activation. Our findings identify PTPN11 as a drug target to combat both intrinsic and acquired resistance to several targeted cancer drugs. Moreover, activated PTPN11 can serve as a biomarker of drug resistance resulting from RTK activation. [Display omitted] •PTPN11 inhibition is synthetic lethal with BRAF inhibitors in BRAF mutant colon cancer•PTPN11 inhibition blocks the effects of EGFR activation by BRAF inhibitors•PTPN11 inhibition is lethal to cancers with activated RTKs•Phosphorylation of PTPN11 is a biomarker of RTK-driven drug resistance in melanoma Using a synthetic lethality screen, Prahallad et al. report that PTPN11 suppression enhances the response to BRAF inhibition in BRAF mutant colon cancers by preventing the effects of receptor tyrosine kinase reactivation. These findings identify PTPN11 as a drug target to combat both intrinsic and acquired resistance to targeted cancer drugs. |
| Author | Gambino, Valentina Beijersbergen, Roderick L. Bardelli, Alberto Willems, Stefan M. Bernards, Rene Germano, Giovanni Prahallad, Anirudh Heynen, Guus J.J.E. Di Nicolantonio, Federica Evers, Bastiaan Vecchione, Loredana Lieftink, Cor |
| Author_xml | – sequence: 1 givenname: Anirudh surname: Prahallad fullname: Prahallad, Anirudh organization: Cancer Genomics Centre Netherlands, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, the Netherlands – sequence: 2 givenname: Guus J.J.E. surname: Heynen fullname: Heynen, Guus J.J.E. organization: Cancer Genomics Centre Netherlands, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, the Netherlands – sequence: 3 givenname: Giovanni surname: Germano fullname: Germano, Giovanni organization: Candiolo Cancer Institute – FPO, IRCCS, Str. prov. 142 Km 3.95, 10060 Candiolo, Torino, Italy – sequence: 4 givenname: Stefan M. surname: Willems fullname: Willems, Stefan M. organization: Cancer Genomics Centre Netherlands, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, the Netherlands – sequence: 5 givenname: Bastiaan surname: Evers fullname: Evers, Bastiaan organization: Cancer Genomics Centre Netherlands, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, the Netherlands – sequence: 6 givenname: Loredana surname: Vecchione fullname: Vecchione, Loredana organization: Cancer Genomics Centre Netherlands, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, the Netherlands – sequence: 7 givenname: Valentina surname: Gambino fullname: Gambino, Valentina organization: Cancer Genomics Centre Netherlands, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, the Netherlands – sequence: 8 givenname: Cor surname: Lieftink fullname: Lieftink, Cor organization: Cancer Genomics Centre Netherlands, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, the Netherlands – sequence: 9 givenname: Roderick L. surname: Beijersbergen fullname: Beijersbergen, Roderick L. organization: Cancer Genomics Centre Netherlands, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, the Netherlands – sequence: 10 givenname: Federica surname: Di Nicolantonio fullname: Di Nicolantonio, Federica organization: Candiolo Cancer Institute – FPO, IRCCS, Str. prov. 142 Km 3.95, 10060 Candiolo, Torino, Italy – sequence: 11 givenname: Alberto surname: Bardelli fullname: Bardelli, Alberto organization: Candiolo Cancer Institute – FPO, IRCCS, Str. prov. 142 Km 3.95, 10060 Candiolo, Torino, Italy – sequence: 12 givenname: Rene surname: Bernards fullname: Bernards, Rene email: r.bernards@nki.nl organization: Cancer Genomics Centre Netherlands, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, the Netherlands |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/26365186$$D View this record in MEDLINE/PubMed |
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| Snippet | Most BRAF (V600E) mutant melanomas are sensitive to selective BRAF inhibitors, but BRAF mutant colon cancers are intrinsically resistant to these drugs because... Most BRAF (V600E) mutant melanomas are sensitive to selective BRAF inhibitors, but BRAF mutant colon cancers are intrinsically resistant to these drugs because... |
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| SubjectTerms | Animals Antineoplastic Agents - pharmacology Cell Line, Tumor Colonic Neoplasms - drug therapy Colonic Neoplasms - genetics Colonic Neoplasms - metabolism Colonic Neoplasms - pathology Drug Resistance, Neoplasm - drug effects Drug Resistance, Neoplasm - genetics Gene Expression Regulation, Neoplastic Genetic Vectors Genomic Library High-Throughput Nucleotide Sequencing Humans Indoles - pharmacology Lentivirus - genetics MAP Kinase Signaling System Melanoma - drug therapy Melanoma - genetics Melanoma - metabolism Melanoma - pathology Mice Mice, Inbred NOD Protein Tyrosine Phosphatase, Non-Receptor Type 11 - antagonists & inhibitors Protein Tyrosine Phosphatase, Non-Receptor Type 11 - genetics Protein Tyrosine Phosphatase, Non-Receptor Type 11 - metabolism Proto-Oncogene Proteins B-raf - genetics Proto-Oncogene Proteins B-raf - metabolism ras Proteins - genetics ras Proteins - metabolism Receptor, Epidermal Growth Factor - genetics Receptor, Epidermal Growth Factor - metabolism RNA, Small Interfering - genetics RNA, Small Interfering - metabolism Sulfonamides - pharmacology Transduction, Genetic Xenograft Model Antitumor Assays |
| Title | PTPN11 Is a Central Node in Intrinsic and Acquired Resistance to Targeted Cancer Drugs |
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