Abstract

The main cause of cervical squamous cell carcinoma (SCC) is the viral integration of human papillomavirus (HPV) to the epithelial cells that leads to genomic instability. This instability leads to gain and over-expression of Oncostatin M receptor (OSMR) in advanced SCC which is associated with significantly worse clinical outcome (1). Cervical SCC cells that over-express OSMR show enhanced responsiveness to its major ligand Oncostatin-M (OSM), which in turn, mediates multiple pro-malignant effects, including a pro-angiogenic phenotype, increased cell migration, invasion, epithelial to mesenchymal transition, metastasis and immune cell recruitment (2, 3). OSMR overexpressing cells are able to trigger OSM secretion from monocytes and macrophages in vitro, to create a niche that promotes the angiogenic switch through hypoxia signalling pathways. OSMR overexpression is linked with the expression of several genes associated with tumour associated macrophages and an immunosuppressive tumour microenvironment (TME) in SCCs. In order to study the role of OSMR in SCCs and the TME , we have examined the effect of syngeneic mouse SCC cell lines with either overexpression or loss of OSMR in wild-type and OSMR knock-out mice by using 18 marker immune cell fluorescence-activated cell sorting (FACS) panel to characterize multiple populations of lymphocytes and myeloid cells. These studies will underpin our assessment of OSMR as a potential therapeutic target in SCCs.