Abstract
Growth hormone-releasing hormone (GHRH) can act as a potent growth factor in various cancers. The mitogenic activity of this neuropeptide is exerted through binding to the pituitary type receptors (GHRH-R) or their splice variants (SV). In the present work, we studied whether this hormone can activate the JAK2/STAT3 pathway which plays a crucial role in cancer cell proliferation and is also linked to carcinogenesis. We transfected HeLa human cervical cancer cells, which are not sensitive to GHRH analogs with the pGHRH-R. Transfected cells responded to the GHRH or its antagonist with an increase or a decrease in proliferation, respectively. These results were confirmed by the expression of proliferating cell nuclear antigen. We then showed that these effects are linked to the activation of the JAK2/STAT3 pathway. Our work demonstrates the activation of JAK/STAT3 pathway by GHRH and sheds further light to the mechanisms of the antitumorogenic action of GHRH antagonists.
Original language | English (US) |
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Pages (from-to) | 959-964 |
Number of pages | 6 |
Journal | Cellular and Molecular Life Sciences |
Volume | 67 |
Issue number | 6 |
DOIs | |
State | Published - Mar 2010 |
Keywords
- GHRH
- Ghrh receptor
- JAK2/STAT3
ASJC Scopus subject areas
- Cell Biology
- Molecular Biology
- Molecular Medicine
- Pharmacology
- Cellular and Molecular Neuroscience
- Medicine(all)