Granulocyte colony-stimulating factor receptor signalling via Janus kinase 2/signal transducer and activator of transcription 3 in ovarian cancer |
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| Authors: | J Kumar F W Fraser C Riley N Ahmed D R McCulloch A C Ward |
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| Affiliation: | 1School of Medicine, Deakin University, Geelong, Victoria 3216, Australia;2Strategic Research Centre in Molecular and Medical Research, Deakin University, Geelong, Victoria 3216, Australia;3Women''s Cancer Research Centre, Royal Women''s Hospital, Parkville, Victoria 3052, Australia;4Department of Obstetrics and Gynaecology, University of Melbourne, Parkville, Victoria 3052, Australia |
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| Abstract: | Background: Ovarian cancer remains a major cause of cancer mortality in women, with only limited understanding of disease aetiology at the molecular level. Granulocyte colony-stimulating factor (G-CSF) is a key regulator of both normal and emergency haematopoiesis, and is used clinically to aid haematopoietic recovery following ablative therapies for a variety of solid tumours including ovarian cancer.Methods: The expression of G-CSF and its receptor, G-CSFR, was examined in primary ovarian cancer samples and a panel of ovarian cancer cell lines, and the effects of G-CSF treatment on proliferation, migration and survival were determined.Results: G-CSFR was predominantly expressed in high-grade serous ovarian epithelial tumour samples and a subset of ovarian cancer cell lines. Stimulation of G-CSFR-expressing ovarian epithelial cancer cells with G-CSF led to increased migration and survival, including against chemotherapy-induced apoptosis. The effects of G-CSF were mediated by signalling via the downstream JAK2/STAT3 pathway.Conclusion: This study suggests that G-CSF has the potential to impact on ovarian cancer pathogenesis, and that G-CSFR expression status should be considered in determining appropriate therapy. |
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| Keywords: | ovarian cancer cytokine cytokine receptor JAK/STAT G-CSF G-CSFR STAT3 |
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