Oncostatin M Receptor-Targeted Antibodies Suppress STAT3 Signaling and Inhibit Ovarian Cancer Growth
Although patients with advanced ovarian cancer may respond initially to treatment, disease relapse is common, and nearly 50% of patients do not survive beyond five years, indicating an urgent need for improved therapies. To identify new therapeutic targets, we performed single-cell and nuclear RNA-s...
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| Published in: | Cancer research (Chicago, Ill.) Vol. 81; no. 20; p. 5336 |
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| Main Authors: | , , , , , , , , , , , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
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United States
15.10.2021
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| ISSN: | 1538-7445, 1538-7445 |
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| Abstract | Although patients with advanced ovarian cancer may respond initially to treatment, disease relapse is common, and nearly 50% of patients do not survive beyond five years, indicating an urgent need for improved therapies. To identify new therapeutic targets, we performed single-cell and nuclear RNA-seq data set analyses on 17 human ovarian cancer specimens, revealing the oncostatin M receptor (OSMR) as highly expressed in ovarian cancer cells. Conversely, oncostatin M (OSM), the ligand of OSMR, was highly expressed by tumor-associated macrophages and promoted proliferation and metastasis in cancer cells. Ovarian cancer cell lines and additional patient samples also exhibited elevated levels of OSMR when compared with other cell types in the tumor microenvironment or to normal ovarian tissue samples. OSMR was found to be important for ovarian cancer cell proliferation and migration. Binding of OSM to OSMR caused OSMR-IL6ST dimerization, which is required to produce oncogenic signaling cues for prolonged STAT3 activation. Human monoclonal antibody clones B14 and B21 directed to the extracellular domain of OSMR abrogated OSM-induced OSMR-IL6ST heterodimerization, promoted the internalization and degradation of OSMR, and effectively blocked OSMR-mediated signaling
. Importantly, these antibody clones inhibited the growth of ovarian cancer cells
and
by suppressing oncogenic signaling through OSMR and STAT3 activation. Collectively, this study provides a proof of principle that anti-OSMR antibody can mediate disruption of OSM-induced OSMR-IL6ST dimerization and oncogenic signaling, thus documenting the preclinical therapeutic efficacy of human OSMR antagonist antibodies for immunotherapy in ovarian cancer. SIGNIFICANCE: This study uncovers a role for OSMR in promoting ovarian cancer cell proliferation and metastasis by activating STAT3 signaling and demonstrates the preclinical efficacy of antibody-based OSMR targeting for ovarian cancer treatment. |
|---|---|
| AbstractList | Although patients with advanced ovarian cancer may respond initially to treatment, disease relapse is common, and nearly 50% of patients do not survive beyond five years, indicating an urgent need for improved therapies. To identify new therapeutic targets, we performed single-cell and nuclear RNA-seq data set analyses on 17 human ovarian cancer specimens, revealing the oncostatin M receptor (OSMR) as highly expressed in ovarian cancer cells. Conversely, oncostatin M (OSM), the ligand of OSMR, was highly expressed by tumor-associated macrophages and promoted proliferation and metastasis in cancer cells. Ovarian cancer cell lines and additional patient samples also exhibited elevated levels of OSMR when compared with other cell types in the tumor microenvironment or to normal ovarian tissue samples. OSMR was found to be important for ovarian cancer cell proliferation and migration. Binding of OSM to OSMR caused OSMR-IL6ST dimerization, which is required to produce oncogenic signaling cues for prolonged STAT3 activation. Human monoclonal antibody clones B14 and B21 directed to the extracellular domain of OSMR abrogated OSM-induced OSMR-IL6ST heterodimerization, promoted the internalization and degradation of OSMR, and effectively blocked OSMR-mediated signaling
. Importantly, these antibody clones inhibited the growth of ovarian cancer cells
and
by suppressing oncogenic signaling through OSMR and STAT3 activation. Collectively, this study provides a proof of principle that anti-OSMR antibody can mediate disruption of OSM-induced OSMR-IL6ST dimerization and oncogenic signaling, thus documenting the preclinical therapeutic efficacy of human OSMR antagonist antibodies for immunotherapy in ovarian cancer. SIGNIFICANCE: This study uncovers a role for OSMR in promoting ovarian cancer cell proliferation and metastasis by activating STAT3 signaling and demonstrates the preclinical efficacy of antibody-based OSMR targeting for ovarian cancer treatment. Although patients with advanced ovarian cancer may respond initially to treatment, disease relapse is common, and nearly 50% of patients do not survive beyond five years, indicating an urgent need for improved therapies. To identify new therapeutic targets, we performed single-cell and nuclear RNA-seq data set analyses on 17 human ovarian cancer specimens, revealing the oncostatin M receptor (OSMR) as highly expressed in ovarian cancer cells. Conversely, oncostatin M (OSM), the ligand of OSMR, was highly expressed by tumor-associated macrophages and promoted proliferation and metastasis in cancer cells. Ovarian cancer cell lines and additional patient samples also exhibited elevated levels of OSMR when compared with other cell types in the tumor microenvironment or to normal ovarian tissue samples. OSMR was found to be important for ovarian cancer cell proliferation and migration. Binding of OSM to OSMR caused OSMR-IL6ST dimerization, which is required to produce oncogenic signaling cues for prolonged STAT3 activation. Human monoclonal antibody clones B14 and B21 directed to the extracellular domain of OSMR abrogated OSM-induced OSMR-IL6ST heterodimerization, promoted the internalization and degradation of OSMR, and effectively blocked OSMR-mediated signaling in vitro. Importantly, these antibody clones inhibited the growth of ovarian cancer cells in vitro and in vivo by suppressing oncogenic signaling through OSMR and STAT3 activation. Collectively, this study provides a proof of principle that anti-OSMR antibody can mediate disruption of OSM-induced OSMR-IL6ST dimerization and oncogenic signaling, thus documenting the preclinical therapeutic efficacy of human OSMR antagonist antibodies for immunotherapy in ovarian cancer. SIGNIFICANCE: This study uncovers a role for OSMR in promoting ovarian cancer cell proliferation and metastasis by activating STAT3 signaling and demonstrates the preclinical efficacy of antibody-based OSMR targeting for ovarian cancer treatment.Although patients with advanced ovarian cancer may respond initially to treatment, disease relapse is common, and nearly 50% of patients do not survive beyond five years, indicating an urgent need for improved therapies. To identify new therapeutic targets, we performed single-cell and nuclear RNA-seq data set analyses on 17 human ovarian cancer specimens, revealing the oncostatin M receptor (OSMR) as highly expressed in ovarian cancer cells. Conversely, oncostatin M (OSM), the ligand of OSMR, was highly expressed by tumor-associated macrophages and promoted proliferation and metastasis in cancer cells. Ovarian cancer cell lines and additional patient samples also exhibited elevated levels of OSMR when compared with other cell types in the tumor microenvironment or to normal ovarian tissue samples. OSMR was found to be important for ovarian cancer cell proliferation and migration. Binding of OSM to OSMR caused OSMR-IL6ST dimerization, which is required to produce oncogenic signaling cues for prolonged STAT3 activation. Human monoclonal antibody clones B14 and B21 directed to the extracellular domain of OSMR abrogated OSM-induced OSMR-IL6ST heterodimerization, promoted the internalization and degradation of OSMR, and effectively blocked OSMR-mediated signaling in vitro. Importantly, these antibody clones inhibited the growth of ovarian cancer cells in vitro and in vivo by suppressing oncogenic signaling through OSMR and STAT3 activation. Collectively, this study provides a proof of principle that anti-OSMR antibody can mediate disruption of OSM-induced OSMR-IL6ST dimerization and oncogenic signaling, thus documenting the preclinical therapeutic efficacy of human OSMR antagonist antibodies for immunotherapy in ovarian cancer. SIGNIFICANCE: This study uncovers a role for OSMR in promoting ovarian cancer cell proliferation and metastasis by activating STAT3 signaling and demonstrates the preclinical efficacy of antibody-based OSMR targeting for ovarian cancer treatment. |
| Author | McAllister, Donna M Kadamberi, Ishaque P Ku, Zhiqiang Li, Yongsheng Geethadevi, Anjali Sun, Yunguang Chaluvally-Raghavan, Pradeep Xiong, Wei Pradeep, Sunila Gupta, Prachi Nair, Ajay Dwinell, Michael B Parashar, Deepak Rui, Hallgeir George, Jasmine Bradley, William H Schwabe, Robert F Zhang, Ningyan An, Zhiqiang Deng, Hui Rader, Janet S |
| Author_xml | – sequence: 1 givenname: Anjali orcidid: 0000-0001-5486-7919 surname: Geethadevi fullname: Geethadevi, Anjali organization: Medical College of Wisconsin Cancer Center, Milwaukee, Wisconsin – sequence: 2 givenname: Ajay orcidid: 0000-0003-4521-5614 surname: Nair fullname: Nair, Ajay organization: Department of Medicine, Columbia University, New York, New York – sequence: 3 givenname: Deepak orcidid: 0000-0002-5062-8950 surname: Parashar fullname: Parashar, Deepak organization: Medical College of Wisconsin Cancer Center, Milwaukee, Wisconsin – sequence: 4 givenname: Zhiqiang surname: Ku fullname: Ku, Zhiqiang organization: Texas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, The University of Texas Health Science Center, Houston, Texas – sequence: 5 givenname: Wei surname: Xiong fullname: Xiong, Wei organization: Texas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, The University of Texas Health Science Center, Houston, Texas – sequence: 6 givenname: Hui surname: Deng fullname: Deng, Hui organization: Texas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, The University of Texas Health Science Center, Houston, Texas – sequence: 7 givenname: Yongsheng orcidid: 0000-0003-1914-0727 surname: Li fullname: Li, Yongsheng organization: Key Laboratory of Tropical Translational Medicine of Ministry of Education, College of Biomedical Information and Engineering, Hainan Medical University, Haikou, China – sequence: 8 givenname: Jasmine surname: George fullname: George, Jasmine organization: Medical College of Wisconsin Cancer Center, Milwaukee, Wisconsin – sequence: 9 givenname: Donna M orcidid: 0000-0001-7332-1292 surname: McAllister fullname: McAllister, Donna M organization: Department of Microbiology and Immunology, Medical College of Wisconsin, Milwaukee, Wisconsin – sequence: 10 givenname: Yunguang orcidid: 0000-0003-4004-9514 surname: Sun fullname: Sun, Yunguang organization: Department of Pathology, Medical College of Wisconsin, Milwaukee, Wisconsin – sequence: 11 givenname: Ishaque P surname: Kadamberi fullname: Kadamberi, Ishaque P organization: Medical College of Wisconsin Cancer Center, Milwaukee, Wisconsin – sequence: 12 givenname: Prachi surname: Gupta fullname: Gupta, Prachi organization: Medical College of Wisconsin Cancer Center, Milwaukee, Wisconsin – sequence: 13 givenname: Michael B surname: Dwinell fullname: Dwinell, Michael B organization: Department of Microbiology and Immunology, Medical College of Wisconsin, Milwaukee, Wisconsin – sequence: 14 givenname: William H surname: Bradley fullname: Bradley, William H organization: Department of Obstetrics and Gynecology, Medical College of Wisconsin, Milwaukee, Wisconsin – sequence: 15 givenname: Janet S orcidid: 0000-0001-7031-3385 surname: Rader fullname: Rader, Janet S organization: Department of Obstetrics and Gynecology, Medical College of Wisconsin, Milwaukee, Wisconsin – sequence: 16 givenname: Hallgeir surname: Rui fullname: Rui, Hallgeir organization: Department of Pathology, Medical College of Wisconsin, Milwaukee, Wisconsin – sequence: 17 givenname: Robert F surname: Schwabe fullname: Schwabe, Robert F organization: Institute of Human Nutrition, Columbia University, New York, New York – sequence: 18 givenname: Ningyan orcidid: 0000-0002-4348-2180 surname: Zhang fullname: Zhang, Ningyan organization: Texas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, The University of Texas Health Science Center, Houston, Texas – sequence: 19 givenname: Sunila orcidid: 0000-0003-2441-7727 surname: Pradeep fullname: Pradeep, Sunila organization: Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin – sequence: 20 givenname: Zhiqiang surname: An fullname: An, Zhiqiang email: pchaluvally@mcw.edu, Zhiqiang.An@uth.tmc.edu organization: Texas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, The University of Texas Health Science Center, Houston, Texas. pchaluvally@mcw.edu Zhiqiang.An@uth.tmc.edu – sequence: 21 givenname: Pradeep orcidid: 0000-0002-8268-3460 surname: Chaluvally-Raghavan fullname: Chaluvally-Raghavan, Pradeep email: pchaluvally@mcw.edu, Zhiqiang.An@uth.tmc.edu organization: Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/34380633$$D View this record in MEDLINE/PubMed |
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| Snippet | Although patients with advanced ovarian cancer may respond initially to treatment, disease relapse is common, and nearly 50% of patients do not survive beyond... |
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| SubjectTerms | Animals Antibodies, Monoclonal - pharmacology Apoptosis Biomarkers, Tumor - genetics Biomarkers, Tumor - metabolism Cancer-Associated Fibroblasts - immunology Cell Proliferation Cytokine Receptor gp130 - genetics Cytokine Receptor gp130 - metabolism Female Gene Expression Regulation, Neoplastic - drug effects Humans Mice Mice, Nude Neoplasm Metastasis Oncostatin M - genetics Oncostatin M - metabolism Oncostatin M Receptor beta Subunit - antagonists & inhibitors Oncostatin M Receptor beta Subunit - immunology Oncostatin M Receptor beta Subunit - metabolism Ovarian Neoplasms - immunology Ovarian Neoplasms - metabolism Ovarian Neoplasms - pathology Ovarian Neoplasms - prevention & control Prognosis STAT3 Transcription Factor - antagonists & inhibitors STAT3 Transcription Factor - genetics STAT3 Transcription Factor - metabolism Tumor Cells, Cultured Tumor Microenvironment Xenograft Model Antitumor Assays |
| Title | Oncostatin M Receptor-Targeted Antibodies Suppress STAT3 Signaling and Inhibit Ovarian Cancer Growth |
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