Dataset related to article "Direct effects of octreotide on osteoblast cell proliferation and function"
Creators
- 1. Department of Biomedical Sciences, Humanitas University, Pieve Emanuele (MI), Italy AND Laboratory of Cellular and Molecular Endocrinology, IRCCS Humanitas Research Hospital, Rozzano, Milan, Italy
- 2. National Research Council, Institute of Biosciences and BioResources (CNR-IBBR), Sesto Fiorentino, Italy
- 3. IRCCS Humanitas Research Hospital, Rozzano, Milan, Italy, 5Department of Clinical Sciences and Community Health, University of Milan, Milan, Italy
- 4. Department of Clinical Sciences and Community Health, University of Milan, Milan, Italy AND Endocrinology Unit, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico
- 5. IRCCS Humanitas Research Hospital, Rozzano, Milan, Italy AND National Research Council, Institute of Genetic and Biomedical Research (CNR-IRGB), Milan, Italy
- 6. Department of Biomedical Sciences, Humanitas University, Pieve Emanuele (MI), Italy AND Endocrinology, Diabetology and Andrology Unit, IRCCS Humanitas Research Hospital, Rozzano (MI), Italy
Description
This record contains data related to article" Direct effects of octreotide on osteoblast cell proliferation and function".
Purpose. Octreotide (OCT) is a first-generation somatostatin analog (SSA) used in the treatment of acromegaly and neuroendocrine tumors (NETs). In both diseases, OCT interacts with somatostatin receptors 2 and 5 (SSTR2 and SSTR5), inhibiting hormone hypersecretion and cell proliferation. Skeletal health is an important clinical concern with acromegaly and NETs since acromegalic osteopathy and NET bone metastasis occur in a remarkable number of patients. While OCT’s effect on NET cells has been extensively investigated, its direct action on bone cells remains unknown.
Methods. Here we investigated OCT direct effects on cell proliferation, differentiation, mineralization, and chemoattractant capacity of murine primary osteoblasts and osteoblast cell line MC3T3-E1.
Results. OCT inhibited osteoblasts and MC3T3-E1 cell proliferation (-30% ± 16%, and -22 ± 4%, both p<0.05) and increased MC3T3-E1 cell apoptosis (+76 ± 32%, p<0.05 vs control).
The anti-proliferative action of OCT was mediated by SSTR2 and SSTR5 in MC3T3-E1, while its proapoptotic effect was abrogated in SSTR2-silenced cells. The analysis of genes related to the early and late phases of osteoblast differentiation showed that OCT did not affect Alp, Runx2, Bglap, Spp1, and Sost levels in MC3T3-E1 cells. Similarly, OCT had no effect on ALP activity and mineralization in osteoblasts. In addition, Vegfa expression decreased in OCT-treated MC3T3-E1 cells and OCT inhibited pancreatic NET cell migration towards osteoblast-conditioned medium.
Conclusion.This study provides the first evidence of the direct action of OCT on osteoblasts which may have clinically relevant implications for the management of skeletal health in subjects with acromegaly and metastatic NETs.
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Additional details
Related works
- Is supplement to
- 10.1007/s40618-022-01740-7 (DOI)
- 3502-0172 (ISSN)