Kinome screening for regulators of the estrogen receptor identifies LMTK3 as a new therapeutic target in breast cancer
This report identifies LMTK3 kinase as a regulator of ERα activity. LMTK3 exerts its effects through direct interaction and indirectly through regulation of PKC, AKT and FOXO3's effects on ERα transcription and stability. LMTK3 can modulate tamoxifen responses and is a poor prognostic factor in...
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| Published in | Nature medicine Vol. 17; no. 6; pp. 715 - 719 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
New York
Nature Publishing Group US
01.06.2011
Nature Publishing Group |
| Subjects | |
| Online Access | Get full text |
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| Abstract | This report identifies LMTK3 kinase as a regulator of ERα activity. LMTK3 exerts its effects through direct interaction and indirectly through regulation of PKC, AKT and FOXO3's effects on ERα transcription and stability. LMTK3 can modulate tamoxifen responses and is a poor prognostic factor in human breast cancer.
Therapies targeting estrogen receptor α (ERα, encoded by
ESR1
) have transformed the treatment of breast cancer. However, large numbers of women relapse, highlighting the need for the discovery of new regulatory targets modulating ERα pathways
1
,
2
,
3
,
4
,
5
. An siRNA screen identified kinases whose silencing alters the estrogen response including those previously implicated in regulating ERα activity (such as mitogen-activated protein kinase and AKT). Among the most potent regulators was lemur tyrosine kinase-3 (LMTK3), for which a role has not previously been assigned. In contrast to other modulators of ERα activity, LMTK3 seems to have been subject to Darwinian positive selection, a noteworthy result given the unique susceptibility of humans to ERα
+
breast cancer. LMTK3 acts by decreasing the activity of protein kinase C (PKC) and the phosphorylation of AKT (Ser473), thereby increasing binding of forkhead box O3 (FOXO3) to the
ESR1
promoter. LMTK3 phosphorylated ERα, protecting it from proteasomal degradation
in vitro
. Silencing of LMTK3 reduced tumor volume in an orthotopic mouse model and abrogated proliferation of ERα
+
but not ERα
−
cells, indicative of its role in ERα activity. In human cancers, LMTK3 abundance and intronic polymorphisms were significantly associated with disease-free and overall survival and predicted response to endocrine therapies. These findings yield insights into the natural history of breast cancer in humans and reveal LMTK3 as a new therapeutic target. |
|---|---|
| AbstractList | Therapies targeting estrogen receptor α (ERα, encoded by ESR1) have transformed the treatment of breast cancer. However, large numbers of women relapse, highlighting the need for the discovery of new regulatory targets modulating ERα pathways (1-5). An siRNA screen identified kinases whose silencing alters the estrogen response including those previously implicated in regulating ERα activity (such as mitogen-activated protein kinase and AKT). Among the most potent regulators was lemur tyrosine kinase-3 (LMTK3), for which a role has not previously been assigned. In contrast to other modulators of ERα activity, LMTK3 seems to have been subject to Darwinian positive selection, a noteworthy result given the unique susceptibility of humans to [ERα.sup.+] breast cancer. LMTK3 acts by decreasing the activity of protein kinase C (PKC) and the phosphorylation of AKT (Ser473), thereby increasing binding of forkhead box O3 (FOXO3) to the ESR1 promoter. LMTK3 phosphorylated ERα, protecting it from proteasomal degradation in vitro. Silencing of LMTK3 reduced tumor volume in an orthotopic mouse model and abrogated proliferation of [ERα.sup.+] but not [ERα.sup.-] cells, indicative of its role in ERα activity. In human cancers, LMTK3 abundance and intronic polymorphisms were significantly associated with disease-free and overall survival and predicted response to endocrine therapies. These findings yield insights into the natural history of breast cancer in humans and reveal LMTK3 as a new therapeutic target. Therapies targeting estrogen receptor α (ERα, encoded by ESR1) have transformed the treatment of breast cancer. However, large numbers of women relapse, highlighting the need for the discovery of new regulatory targets modulating ERα pathways. An siRNA screen identified kinases whose silencing alters the estrogen response including those previously implicated in regulating ERα activity (such as mitogen-activated protein kinase and AKT). Among the most potent regulators was lemur tyrosine kinase-3 (LMTK3), for which a role has not previously been assigned. In contrast to other modulators of ERα activity, LMTK3 seems to have been subject to Darwinian positive selection, a noteworthy result given the unique susceptibility of humans to ERα+ breast cancer. LMTK3 acts by decreasing the activity of protein kinase C (PKC) and the phosphorylation of AKT (Ser473), thereby increasing binding of forkhead box O3 (FOXO3) to the ESR1 promoter. LMTK3 phosphorylated ERα, protecting it from proteasomal degradation in vitro. Silencing of LMTK3 reduced tumor volume in an orthotopic mouse model and abrogated proliferation of ERα+ but not ERα- cells, indicative of its role in ERα activity. In human cancers, LMTK3 abundance and intronic polymorphisms were significantly associated with disease-free and overall survival and predicted response to endocrine therapies. These findings yield insights into the natural history of breast cancer in humans and reveal LMTK3 as a new therapeutic target. Therapies targeting estrogen receptor α (ERα, encoded by ESR1) have transformed the treatment of breast cancer. However, large numbers of women relapse, highlighting the need for the discovery of new regulatory targets modulating ERα pathways. An siRNA screen identified kinases whose silencing alters the estrogen response including those previously implicated in regulating ERα activity (such as mitogen-activated protein kinase and AKT). Among the most potent regulators was lemur tyrosine kinase-3 (LMTK3), for which a role has not previously been assigned. In contrast to other modulators of ERα activity, LMTK3 seems to have been subject to Darwinian positive selection, a noteworthy result given the unique susceptibility of humans to ERα+ breast cancer. LMTK3 acts by decreasing the activity of protein kinase C (PKC) and the phosphorylation of AKT (Ser473), thereby increasing binding of forkhead box O3 (FOXO3) to the ESR1 promoter. LMTK3 phosphorylated ERα, protecting it from proteasomal degradation in vitro. Silencing of LMTK3 reduced tumor volume in an orthotopic mouse model and abrogated proliferation of ERα+ but not ERα- cells, indicative of its role in ERα activity. In human cancers, LMTK3 abundance and intronic polymorphisms were significantly associated with disease-free and overall survival and predicted response to endocrine therapies. These findings yield insights into the natural history of breast cancer in humans and reveal LMTK3 as a new therapeutic target.Therapies targeting estrogen receptor α (ERα, encoded by ESR1) have transformed the treatment of breast cancer. However, large numbers of women relapse, highlighting the need for the discovery of new regulatory targets modulating ERα pathways. An siRNA screen identified kinases whose silencing alters the estrogen response including those previously implicated in regulating ERα activity (such as mitogen-activated protein kinase and AKT). Among the most potent regulators was lemur tyrosine kinase-3 (LMTK3), for which a role has not previously been assigned. In contrast to other modulators of ERα activity, LMTK3 seems to have been subject to Darwinian positive selection, a noteworthy result given the unique susceptibility of humans to ERα+ breast cancer. LMTK3 acts by decreasing the activity of protein kinase C (PKC) and the phosphorylation of AKT (Ser473), thereby increasing binding of forkhead box O3 (FOXO3) to the ESR1 promoter. LMTK3 phosphorylated ERα, protecting it from proteasomal degradation in vitro. Silencing of LMTK3 reduced tumor volume in an orthotopic mouse model and abrogated proliferation of ERα+ but not ERα- cells, indicative of its role in ERα activity. In human cancers, LMTK3 abundance and intronic polymorphisms were significantly associated with disease-free and overall survival and predicted response to endocrine therapies. These findings yield insights into the natural history of breast cancer in humans and reveal LMTK3 as a new therapeutic target. This report identifies LMTK3 kinase as a regulator of ERα activity. LMTK3 exerts its effects through direct interaction and indirectly through regulation of PKC, AKT and FOXO3's effects on ERα transcription and stability. LMTK3 can modulate tamoxifen responses and is a poor prognostic factor in human breast cancer. Therapies targeting estrogen receptor α (ERα, encoded by ESR1 ) have transformed the treatment of breast cancer. However, large numbers of women relapse, highlighting the need for the discovery of new regulatory targets modulating ERα pathways 1 , 2 , 3 , 4 , 5 . An siRNA screen identified kinases whose silencing alters the estrogen response including those previously implicated in regulating ERα activity (such as mitogen-activated protein kinase and AKT). Among the most potent regulators was lemur tyrosine kinase-3 (LMTK3), for which a role has not previously been assigned. In contrast to other modulators of ERα activity, LMTK3 seems to have been subject to Darwinian positive selection, a noteworthy result given the unique susceptibility of humans to ERα + breast cancer. LMTK3 acts by decreasing the activity of protein kinase C (PKC) and the phosphorylation of AKT (Ser473), thereby increasing binding of forkhead box O3 (FOXO3) to the ESR1 promoter. LMTK3 phosphorylated ERα, protecting it from proteasomal degradation in vitro . Silencing of LMTK3 reduced tumor volume in an orthotopic mouse model and abrogated proliferation of ERα + but not ERα − cells, indicative of its role in ERα activity. In human cancers, LMTK3 abundance and intronic polymorphisms were significantly associated with disease-free and overall survival and predicted response to endocrine therapies. These findings yield insights into the natural history of breast cancer in humans and reveal LMTK3 as a new therapeutic target. |
| Audience | Academic |
| Author | Filipović, Aleksandra Zhang, Wu Coombes, R Charles Zhang, Hua Castellano, Leandro Stebbing, Justin Tralau-Stewart, Cathy Giamas, Georgios Messier, Walter Ellis, Ian O Lenz, Heinz-Josef Shifa, Belul Assefa Photiou, Andrew Green, Andrew R Jacob, Jimmy Yang, Dongyun Ali, Simak |
| Author_xml | – sequence: 1 givenname: Georgios surname: Giamas fullname: Giamas, Georgios email: g.giamas@imperial.ac.uk organization: Department of Surgery and Cancer, Imperial College London, Hammersmith Hospital Campus – sequence: 2 givenname: Aleksandra surname: Filipović fullname: Filipović, Aleksandra organization: Department of Surgery and Cancer, Imperial College London, Hammersmith Hospital Campus – sequence: 3 givenname: Jimmy surname: Jacob fullname: Jacob, Jimmy organization: Department of Surgery and Cancer, Imperial College London, Hammersmith Hospital Campus – sequence: 4 givenname: Walter surname: Messier fullname: Messier, Walter organization: Evolutionary Genomics, Inc., Lafayette – sequence: 5 givenname: Hua surname: Zhang fullname: Zhang, Hua organization: Department of Surgery and Cancer, Imperial College London, Hammersmith Hospital Campus – sequence: 6 givenname: Dongyun surname: Yang fullname: Yang, Dongyun organization: Division of Medical Oncology, University of Southern California, Norris Comprehensive Cancer Center, Keck School of Medicine – sequence: 7 givenname: Wu surname: Zhang fullname: Zhang, Wu organization: Division of Medical Oncology, University of Southern California, Norris Comprehensive Cancer Center, Keck School of Medicine – sequence: 8 givenname: Belul Assefa surname: Shifa fullname: Shifa, Belul Assefa organization: Department of Surgery and Cancer, Imperial College London, Hammersmith Hospital Campus – sequence: 9 givenname: Andrew surname: Photiou fullname: Photiou, Andrew organization: Department of Surgery and Cancer, Imperial College London, Hammersmith Hospital Campus – sequence: 10 givenname: Cathy surname: Tralau-Stewart fullname: Tralau-Stewart, Cathy organization: Drug Discovery Centre, Imperial College London, Biochemistry Building, South Kensington Campus, London, UK – sequence: 11 givenname: Leandro surname: Castellano fullname: Castellano, Leandro organization: Department of Surgery and Cancer, Imperial College London, Hammersmith Hospital Campus – sequence: 12 givenname: Andrew R surname: Green fullname: Green, Andrew R organization: Histopathology, School of Molecular Medical Sciences, University of Nottingham and Nottingham University NHS Hospital Trust – sequence: 13 givenname: R Charles surname: Coombes fullname: Coombes, R Charles organization: Department of Surgery and Cancer, Imperial College London, Hammersmith Hospital Campus – sequence: 14 givenname: Ian O surname: Ellis fullname: Ellis, Ian O organization: Histopathology, School of Molecular Medical Sciences, University of Nottingham and Nottingham University NHS Hospital Trust – sequence: 15 givenname: Simak surname: Ali fullname: Ali, Simak organization: Department of Surgery and Cancer, Imperial College London, Hammersmith Hospital Campus – sequence: 16 givenname: Heinz-Josef surname: Lenz fullname: Lenz, Heinz-Josef organization: Division of Medical Oncology, University of Southern California, Norris Comprehensive Cancer Center, Keck School of Medicine – sequence: 17 givenname: Justin surname: Stebbing fullname: Stebbing, Justin email: j.stebbing@imperial.ac.uk organization: Department of Surgery and Cancer, Imperial College London, Hammersmith Hospital Campus |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/21602804$$D View this record in MEDLINE/PubMed |
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| Snippet | This report identifies LMTK3 kinase as a regulator of ERα activity. LMTK3 exerts its effects through direct interaction and indirectly through regulation of... Therapies targeting estrogen receptor α (ERα, encoded by ESR1) have transformed the treatment of breast cancer. However, large numbers of women relapse,... |
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| Title | Kinome screening for regulators of the estrogen receptor identifies LMTK3 as a new therapeutic target in breast cancer |
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