Dual‐targeting therapy against HER3/MET in human colorectal cancers
Background Colorectal cancer (CRC) is the most common malignancy in the world, and novel molecular targeted therapies for CRC have been vigorously pursued. We searched for novel combination therapies based on the expression patterns of membrane proteins in CRC cell lines. Results A positive correlat...
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| Published in | Cancer medicine (Malden, MA) Vol. 12; no. 8; pp. 9684 - 9696 |
|---|---|
| Main Authors | , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
John Wiley & Sons, Inc
01.04.2023
John Wiley and Sons Inc Wiley |
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| Abstract | Background
Colorectal cancer (CRC) is the most common malignancy in the world, and novel molecular targeted therapies for CRC have been vigorously pursued. We searched for novel combination therapies based on the expression patterns of membrane proteins in CRC cell lines.
Results
A positive correlation was observed between the expression of human pidermal growth factor receptor (HER) 3 and mesenchymal‐to‐epithelial transition factor (MET) on the cell surface of CRC cell lines. The brief stimulation of HER3/MET‐high SW1116 CRC cells with both neuregulin‐1 (NRG1) and hepatocyte growth factor enhanced ERK phosphorylation and cell proliferation more than each stimulation alone. In addition, a prolonged NRG1 stimulation resulted in the tyrosine phosphorylation of MET. In this context, the Forkhead Box protein M1 (FOXM1)‐regulated tyrosine phosphorylation of MET by NRG1 was demonstrated, suggesting the existence of a signaling pathway mediated by FOXM1 upon the NRG1 stimulation. Since the co‐expression of HER3 and MET was also demonstrated in in vivo CRC tissues by immunohistochemistry, we investigated whether the co‐inhibition of HER3 and MET could be an effective therapy for CRC. We established HER3‐and/or MET‐KO SW1116 cell lines, and HER3/MET‐double KO resulted in the inhibition of in vitro cell proliferation and in vivo tumor growth in nude mice by SW1116 cells. Furthermore, the combination of patritumab, an anti‐HER3 fully human mAb, and PHA665752, a MET inhibitor, markedly inhibited in vitro cell proliferation, 3D‐colony formation, and in vivo tumor growth in nude mice by SW1116 cells
Conclusion
The dual targeting of HER3/MET has potential as CRC therapy.
The present study demonstrated that HER3 and MET were not directly associated with each other in CRC but cooperated for the cellular and tumor growth of CRC. In this context, the combination of anti‐HER3 (patritumab) and anti‐MET (PHA665752) drugs was definitely effective against HER3/MET‐high SW1116 CRC cells, indicating the potential of the dual inhibition of HER3 and MET as targeting therapy in human CRC. |
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| AbstractList | Background
Colorectal cancer (CRC) is the most common malignancy in the world, and novel molecular targeted therapies for CRC have been vigorously pursued. We searched for novel combination therapies based on the expression patterns of membrane proteins in CRC cell lines.
Results
A positive correlation was observed between the expression of human pidermal growth factor receptor (HER) 3 and mesenchymal‐to‐epithelial transition factor (MET) on the cell surface of CRC cell lines. The brief stimulation of HER3/MET‐high SW1116 CRC cells with both neuregulin‐1 (NRG1) and hepatocyte growth factor enhanced ERK phosphorylation and cell proliferation more than each stimulation alone. In addition, a prolonged NRG1 stimulation resulted in the tyrosine phosphorylation of MET. In this context, the Forkhead Box protein M1 (FOXM1)‐regulated tyrosine phosphorylation of MET by NRG1 was demonstrated, suggesting the existence of a signaling pathway mediated by FOXM1 upon the NRG1 stimulation. Since the co‐expression of HER3 and MET was also demonstrated in in vivo CRC tissues by immunohistochemistry, we investigated whether the co‐inhibition of HER3 and MET could be an effective therapy for CRC. We established HER3‐and/or MET‐KO SW1116 cell lines, and HER3/MET‐double KO resulted in the inhibition of in vitro cell proliferation and in vivo tumor growth in nude mice by SW1116 cells. Furthermore, the combination of patritumab, an anti‐HER3 fully human mAb, and PHA665752, a MET inhibitor, markedly inhibited in vitro cell proliferation, 3D‐colony formation, and in vivo tumor growth in nude mice by SW1116 cells
Conclusion
The dual targeting of HER3/MET has potential as CRC therapy.
The present study demonstrated that HER3 and MET were not directly associated with each other in CRC but cooperated for the cellular and tumor growth of CRC. In this context, the combination of anti‐HER3 (patritumab) and anti‐MET (PHA665752) drugs was definitely effective against HER3/MET‐high SW1116 CRC cells, indicating the potential of the dual inhibition of HER3 and MET as targeting therapy in human CRC. Abstract Background Colorectal cancer (CRC) is the most common malignancy in the world, and novel molecular targeted therapies for CRC have been vigorously pursued. We searched for novel combination therapies based on the expression patterns of membrane proteins in CRC cell lines. Results A positive correlation was observed between the expression of human pidermal growth factor receptor (HER) 3 and mesenchymal‐to‐epithelial transition factor (MET) on the cell surface of CRC cell lines. The brief stimulation of HER3/MET‐high SW1116 CRC cells with both neuregulin‐1 (NRG1) and hepatocyte growth factor enhanced ERK phosphorylation and cell proliferation more than each stimulation alone. In addition, a prolonged NRG1 stimulation resulted in the tyrosine phosphorylation of MET. In this context, the Forkhead Box protein M1 (FOXM1)‐regulated tyrosine phosphorylation of MET by NRG1 was demonstrated, suggesting the existence of a signaling pathway mediated by FOXM1 upon the NRG1 stimulation. Since the co‐expression of HER3 and MET was also demonstrated in in vivo CRC tissues by immunohistochemistry, we investigated whether the co‐inhibition of HER3 and MET could be an effective therapy for CRC. We established HER3‐and/or MET‐KO SW1116 cell lines, and HER3/MET‐double KO resulted in the inhibition of in vitro cell proliferation and in vivo tumor growth in nude mice by SW1116 cells. Furthermore, the combination of patritumab, an anti‐HER3 fully human mAb, and PHA665752, a MET inhibitor, markedly inhibited in vitro cell proliferation, 3D‐colony formation, and in vivo tumor growth in nude mice by SW1116 cells Conclusion The dual targeting of HER3/MET has potential as CRC therapy. The present study demonstrated that HER3 and MET were not directly associated with each other in CRC but cooperated for the cellular and tumor growth of CRC. In this context, the combination of anti‐HER3 (patritumab) and anti‐MET (PHA665752) drugs was definitely effective against HER3/MET‐high SW1116 CRC cells, indicating the potential of the dual inhibition of HER3 and MET as targeting therapy in human CRC. BACKGROUNDColorectal cancer (CRC) is the most common malignancy in the world, and novel molecular targeted therapies for CRC have been vigorously pursued. We searched for novel combination therapies based on the expression patterns of membrane proteins in CRC cell lines. RESULTSA positive correlation was observed between the expression of human pidermal growth factor receptor (HER) 3 and mesenchymal-to-epithelial transition factor (MET) on the cell surface of CRC cell lines. The brief stimulation of HER3/MET-high SW1116 CRC cells with both neuregulin-1 (NRG1) and hepatocyte growth factor enhanced ERK phosphorylation and cell proliferation more than each stimulation alone. In addition, a prolonged NRG1 stimulation resulted in the tyrosine phosphorylation of MET. In this context, the Forkhead Box protein M1 (FOXM1)-regulated tyrosine phosphorylation of MET by NRG1 was demonstrated, suggesting the existence of a signaling pathway mediated by FOXM1 upon the NRG1 stimulation. Since the co-expression of HER3 and MET was also demonstrated in in vivo CRC tissues by immunohistochemistry, we investigated whether the co-inhibition of HER3 and MET could be an effective therapy for CRC. We established HER3-and/or MET-KO SW1116 cell lines, and HER3/MET-double KO resulted in the inhibition of in vitro cell proliferation and in vivo tumor growth in nude mice by SW1116 cells. Furthermore, the combination of patritumab, an anti-HER3 fully human mAb, and PHA665752, a MET inhibitor, markedly inhibited in vitro cell proliferation, 3D-colony formation, and in vivo tumor growth in nude mice by SW1116 cells CONCLUSION: The dual targeting of HER3/MET has potential as CRC therapy. BackgroundColorectal cancer (CRC) is the most common malignancy in the world, and novel molecular targeted therapies for CRC have been vigorously pursued. We searched for novel combination therapies based on the expression patterns of membrane proteins in CRC cell lines.ResultsA positive correlation was observed between the expression of human pidermal growth factor receptor (HER) 3 and mesenchymal-to-epithelial transition factor (MET) on the cell surface of CRC cell lines. The brief stimulation of HER3/MET-high SW1116 CRC cells with both neuregulin-1 (NRG1) and hepatocyte growth factor enhanced ERK phosphorylation and cell proliferation more than each stimulation alone. In addition, a prolonged NRG1 stimulation resulted in the tyrosine phosphorylation of MET. In this context, the Forkhead Box protein M1 (FOXM1)-regulated tyrosine phosphorylation of MET by NRG1 was demonstrated, suggesting the existence of a signaling pathway mediated by FOXM1 upon the NRG1 stimulation. Since the co-expression of HER3 and MET was also demonstrated in in vivo CRC tissues by immunohistochemistry, we investigated whether the co-inhibition of HER3 and MET could be an effective therapy for CRC. We established HER3-and/or MET-KO SW1116 cell lines, and HER3/MET-double KO resulted in the inhibition of in vitro cell proliferation and in vivo tumor growth in nude mice by SW1116 cells. Furthermore, the combination of patritumab, an anti-HER3 fully human mAb, and PHA665752, a MET inhibitor, markedly inhibited in vitro cell proliferation, 3D-colony formation, and in vivo tumor growth in nude mice by SW1116 cellsConclusionThe dual targeting of HER3/MET has potential as CRC therapy. Colorectal cancer (CRC) is the most common malignancy in the world, and novel molecular targeted therapies for CRC have been vigorously pursued. We searched for novel combination therapies based on the expression patterns of membrane proteins in CRC cell lines. A positive correlation was observed between the expression of human pidermal growth factor receptor (HER) 3 and mesenchymal-to-epithelial transition factor (MET) on the cell surface of CRC cell lines. The brief stimulation of HER3/MET-high SW1116 CRC cells with both neuregulin-1 (NRG1) and hepatocyte growth factor enhanced ERK phosphorylation and cell proliferation more than each stimulation alone. In addition, a prolonged NRG1 stimulation resulted in the tyrosine phosphorylation of MET. In this context, the Forkhead Box protein M1 (FOXM1)-regulated tyrosine phosphorylation of MET by NRG1 was demonstrated, suggesting the existence of a signaling pathway mediated by FOXM1 upon the NRG1 stimulation. Since the co-expression of HER3 and MET was also demonstrated in in vivo CRC tissues by immunohistochemistry, we investigated whether the co-inhibition of HER3 and MET could be an effective therapy for CRC. We established HER3-and/or MET-KO SW1116 cell lines, and HER3/MET-double KO resulted in the inhibition of in vitro cell proliferation and in vivo tumor growth in nude mice by SW1116 cells. Furthermore, the combination of patritumab, an anti-HER3 fully human mAb, and PHA665752, a MET inhibitor, markedly inhibited in vitro cell proliferation, 3D-colony formation, and in vivo tumor growth in nude mice by SW1116 cells CONCLUSION: The dual targeting of HER3/MET has potential as CRC therapy. Abstract Background Colorectal cancer (CRC) is the most common malignancy in the world, and novel molecular targeted therapies for CRC have been vigorously pursued. We searched for novel combination therapies based on the expression patterns of membrane proteins in CRC cell lines. Results A positive correlation was observed between the expression of human pidermal growth factor receptor (HER) 3 and mesenchymal‐to‐epithelial transition factor (MET) on the cell surface of CRC cell lines. The brief stimulation of HER3/MET‐high SW1116 CRC cells with both neuregulin‐1 (NRG1) and hepatocyte growth factor enhanced ERK phosphorylation and cell proliferation more than each stimulation alone. In addition, a prolonged NRG1 stimulation resulted in the tyrosine phosphorylation of MET. In this context, the Forkhead Box protein M1 (FOXM1)‐regulated tyrosine phosphorylation of MET by NRG1 was demonstrated, suggesting the existence of a signaling pathway mediated by FOXM1 upon the NRG1 stimulation. Since the co‐expression of HER3 and MET was also demonstrated in in vivo CRC tissues by immunohistochemistry, we investigated whether the co‐inhibition of HER3 and MET could be an effective therapy for CRC. We established HER3‐and/or MET‐KO SW1116 cell lines, and HER3/MET‐double KO resulted in the inhibition of in vitro cell proliferation and in vivo tumor growth in nude mice by SW1116 cells. Furthermore, the combination of patritumab, an anti‐HER3 fully human mAb, and PHA665752, a MET inhibitor, markedly inhibited in vitro cell proliferation, 3D‐colony formation, and in vivo tumor growth in nude mice by SW1116 cells Conclusion The dual targeting of HER3/MET has potential as CRC therapy. |
| Author | Endo, Yuichi Imaida, Takuya Miyake, Rikuto Masuko, Takashi Tomioka, Yoshihisa Okuno, Hideki Masuko, Kazue Yamasaki, Akitaka Akiyama, Yasutoshi Hirotani, Kenji Hara, Yuta Okita, Kouki Okazaki, Shogo |
| AuthorAffiliation | 1 Cell Biology Laboratory, Faculty of Pharmacy Kindai University Osaka Japan 2 Laboratory of Oncology Pharmacy Practice and Science, Graduate School of Pharmaceutical Sciences Tohoku University Sendai‐shi Japan 6 Natural Drug Resources, Faculty of Pharmacy Kindai University Osaka Japan 4 Division of Immunology and Pathobiology, Department of Microbiology Nihon University School of Density Tokyo Japan 5 Early Clinical Development Department, R&D Division Daiichi Sankyo Co., Ltd. Tokyo Japan 3 Production and Manufacturing Carna Biosciences, Inc. Kobe Japan |
| AuthorAffiliation_xml | – name: 3 Production and Manufacturing Carna Biosciences, Inc. Kobe Japan – name: 6 Natural Drug Resources, Faculty of Pharmacy Kindai University Osaka Japan – name: 2 Laboratory of Oncology Pharmacy Practice and Science, Graduate School of Pharmaceutical Sciences Tohoku University Sendai‐shi Japan – name: 5 Early Clinical Development Department, R&D Division Daiichi Sankyo Co., Ltd. Tokyo Japan – name: 4 Division of Immunology and Pathobiology, Department of Microbiology Nihon University School of Density Tokyo Japan – name: 1 Cell Biology Laboratory, Faculty of Pharmacy Kindai University Osaka Japan |
| Author_xml | – sequence: 1 givenname: Akitaka surname: Yamasaki fullname: Yamasaki, Akitaka organization: Tohoku University – sequence: 2 givenname: Rikuto surname: Miyake fullname: Miyake, Rikuto organization: Kindai University – sequence: 3 givenname: Yuta surname: Hara fullname: Hara, Yuta organization: Kindai University – sequence: 4 givenname: Hideki surname: Okuno fullname: Okuno, Hideki organization: Kindai University – sequence: 5 givenname: Takuya surname: Imaida fullname: Imaida, Takuya organization: Kindai University – sequence: 6 givenname: Kouki surname: Okita fullname: Okita, Kouki organization: Carna Biosciences, Inc – sequence: 7 givenname: Shogo surname: Okazaki fullname: Okazaki, Shogo organization: Nihon University School of Density – sequence: 8 givenname: Yasutoshi surname: Akiyama fullname: Akiyama, Yasutoshi organization: Tohoku University – sequence: 9 givenname: Kenji surname: Hirotani fullname: Hirotani, Kenji organization: Daiichi Sankyo Co., Ltd – sequence: 10 givenname: Yuichi surname: Endo fullname: Endo, Yuichi organization: Kindai University – sequence: 11 givenname: Kazue surname: Masuko fullname: Masuko, Kazue organization: Kindai University – sequence: 12 givenname: Takashi orcidid: 0000-0002-2410-2007 surname: Masuko fullname: Masuko, Takashi email: masuko@phar.kindai.ac.jp organization: Kindai University – sequence: 13 givenname: Yoshihisa surname: Tomioka fullname: Tomioka, Yoshihisa organization: Tohoku University |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/36751113$$D View this record in MEDLINE/PubMed |
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| Copyright | 2023 The Authors. published by John Wiley & Sons Ltd. 2023 The Authors. Cancer Medicine published by John Wiley & Sons Ltd. 2023. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
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| Keywords | human epidermal growth factor receptor family Forkhead Box protein M1 colorectal cancer mesenchymal to epithelial transition factor |
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| License | Attribution 2023 The Authors. Cancer Medicine published by John Wiley & Sons Ltd. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
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| Snippet | Background
Colorectal cancer (CRC) is the most common malignancy in the world, and novel molecular targeted therapies for CRC have been vigorously pursued. We... Colorectal cancer (CRC) is the most common malignancy in the world, and novel molecular targeted therapies for CRC have been vigorously pursued. We searched... Abstract Background Colorectal cancer (CRC) is the most common malignancy in the world, and novel molecular targeted therapies for CRC have been vigorously... BackgroundColorectal cancer (CRC) is the most common malignancy in the world, and novel molecular targeted therapies for CRC have been vigorously pursued. We... BACKGROUNDColorectal cancer (CRC) is the most common malignancy in the world, and novel molecular targeted therapies for CRC have been vigorously pursued. We... The present study demonstrated that HER3 and MET were not directly associated with each other in CRC but cooperated for the cellular and tumor growth of CRC.... Abstract Background Colorectal cancer (CRC) is the most common malignancy in the world, and novel molecular targeted therapies for CRC have been vigorously... |
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| SubjectTerms | Animals Antibodies c-Met protein Cancer therapies Cell culture Cell Line, Tumor Cell Proliferation Cell surface Colorectal cancer Colorectal carcinoma Colorectal Neoplasms - drug therapy Colorectal Neoplasms - genetics Colorectal Neoplasms - metabolism Forkhead Box protein M1 Forkhead protein Glycerol Growth factors Hepatocyte growth factor human epidermal growth factor receptor family Humans Immunohistochemistry Kinases Laboratory animals Malignancy Membrane proteins Membranes mesenchymal to epithelial transition factor Mice Mice, Nude Neuregulin 1 Phosphorylation Proteins Signal Transduction Tumors Tyrosine |
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| Title | Dual‐targeting therapy against HER3/MET in human colorectal cancers |
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