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. © 2013 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.
Highlights
Despite a reduction in incidence and mortality rates since the introduction of population-wide screening programmes in developed countries, cervical carcinoma remains the second most common cause of cancer deaths in women worldwide [1]
oncostatin M receptor (OSMR) is a member of the interleukin 6 (IL6) receptor family
We studied the effects of oncostatin M (OSM)–OSMR interactions on the phenotype of cervical squamous cell carcinoma (SCC) cells by using
Summary
Despite a reduction in incidence and mortality rates since the introduction of population-wide screening programmes in developed countries, cervical carcinoma remains the second most common cause of cancer deaths in women worldwide [1]. An important feature of cervical carcinogenesis is genomic instability caused by deregulated expression of HR-HPV oncogenes in proliferating epithelial cells [4] These changes lead to the selection of particular genomic copy number imbalances, which are likely to provide a selective advantage through altered expression of ‘driver’ host genes. We subsequently used gene expression analysis to identify candidate driver genes for which mRNA expression levels were significantly associated with gene copy number [5,17] Among these genes, the oncostatin M receptor (OSMR) and the microRNA processor Drosha were functionally validated and are likely to contribute to the selection of 5p gain in cervical carcinogenesis [5,17,18,19]. While this finding reflects observations in breast carcinomas (see below), it was from a single set of cervical SCC samples and needs to be verified independently
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