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Oncostatin M receptor is a novel therapeutic target in cervical squamous cell carcinoma
Maria M Caffarel1, Nicholas Coleman
1Department of Pathology, University of Cambridge, UK.
Abstract:
Cervical carcinoma is the second most common cause of cancer deaths in women worldwide. Treatments have not changed for decades and survival rates for advanced disease remain low. An exciting new molecular target for the treatment of cervical squamous cell carcinoma (SCC), and possibly for SCCs at other anatomical sites, is the oncostatin M receptor (OSMR). This cell surface cytokine receptor is commonly copy number gained and overexpressed in advanced cervical SCC, changes that are associated with significantly worse clinical outcomes. OSMR overexpression in cervical SCC cells results in enhanced responsiveness to the major ligand oncostatin M (OSM), which induces several pro-malignant effects, including a pro-angiogenic phenotype and increased cell migration and invasiveness. OSMR is a strong candidate for antibody-mediated inhibition, a strategy that has had a major impact on haematological malignancies and various solid tumours such as HER2-positive breast cancers.
Insights
Oncostatin M receptor (OSMR) is overexpressed in cervical squamous cell carcinoma (SCC), driving cancer growth and poor outcomes. Targeting OSMR offers a promising new treatment strategy for advanced cervical cancer.
Area of Science:
- Oncology
- Molecular Biology
- Immunology
Background:
- Cervical carcinoma is a leading cause of cancer deaths in women globally.
- Current treatments for advanced cervical cancer have limited efficacy, with low survival rates.
- The oncostatin M receptor (OSMR) is a novel molecular target identified in cervical squamous cell carcinoma (SCC).
Purpose of the Study:
- To investigate the role of OSMR in the development and progression of cervical SCC.
- To evaluate OSMR as a potential therapeutic target for cervical cancer treatment.
Main Methods:
- Analysis of OSMR copy number gain and overexpression in advanced cervical SCC.
- Assessment of OSMR ligand (OSM) interactions and downstream effects on cancer cells.
- Exploration of antibody-mediated inhibition of OSMR as a therapeutic strategy.
Main Results:
- OSMR is frequently copy number gained and overexpressed in advanced cervical SCC.
- OSMR overexpression correlates with significantly worse clinical outcomes.
- OSM-induced OSMR signaling promotes angiogenesis, migration, and invasiveness in cervical SCC cells.
Conclusions:
- OSMR is a key driver of malignant progression in cervical SCC.
- Targeting OSMR, particularly through antibody-mediated inhibition, represents a promising therapeutic avenue for advanced cervical cancer and potentially other SCCs.
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