The Somatostatin Analogue Octreotide Inhibits Growth of Small Intestine Neuroendocrine Tumour Cells
Octreotide is a widely used synthetic somatostatin analogue that significantly improves the management of neuroendocrine tumours (NETs). Octreotide acts through somatostatin receptors (SSTRs). However, the molecular mechanisms leading to successful disease control or symptom management, especially w...
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| Published in | PloS one Vol. 7; no. 10; p. e48411 |
|---|---|
| Main Authors | , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Public Library of Science
31.10.2012
Public Library of Science (PLoS) |
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| Abstract | Octreotide is a widely used synthetic somatostatin analogue that significantly improves the management of neuroendocrine tumours (NETs). Octreotide acts through somatostatin receptors (SSTRs). However, the molecular mechanisms leading to successful disease control or symptom management, especially when SSTRs levels are low, are largely unknown. We provide novel insights into how octreotide controls NET cells. CNDT2.5 cells were treated from 1 day up to 16 months with octreotide and then were profiled using Affymetrix microarray analysis. Quantitative real-time PCR and western blot analyses were used to validate microarray profiling in silico data. WST-1 cell proliferation assay was applied to evaluate cell growth of CNDT2.5 cells in the presence or absence of 1 µM octreotide at different time points. Moreover, laser capture microdissected tumour cells and paraffin embedded tissue slides from SI-NETs at different stages of disease were used to identify transcriptional and translational expression. Microarrays analyses did not reveal relevant changes in SSTR expression levels. Unexpectedly, six novel genes were found to be upregulated by octreotide: annexin A1 (ANXA1), rho GTPase-activating protein 18 (ARHGAP18), epithelial membrane protein 1 (EMP1), growth/differentiation factor 15 (GDF15), TGF-beta type II receptor (TGFBR2) and tumour necrosis factor (ligand) superfamily member 15 (TNFSF15). Furthermore, these novel genes were expressed in tumour tissues at transcript and protein levels. We suggest that octreotide may use a potential novel framework to exert its beneficial effect as a drug and to convey its action on neuroendocrine cells. Thus, six novel genes may regulate cell growth and differentiation in normal and tumour neuroendocrine cells and have a role in a novel octreotide mechanism system. |
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| AbstractList | Octreotide is a widely used synthetic somatostatin analogue that significantly improves the management of neuroendocrine tumours (NETs). Octreotide acts through somatostatin receptors (SSTRs). However, the molecular mechanisms leading to successful disease control or symptom management, especially when SSTRs levels are low, are largely unknown. We provide novel insights into how octreotide controls NET cells. CNDT2.5 cells were treated from 1 day up to 16 months with octreotide and then were profiled using Affymetrix microarray analysis. Quantitative real-time PCR and western blot analyses were used to validate microarray profiling in silico data. WST-1 cell proliferation assay was applied to evaluate cell growth of CNDT2.5 cells in the presence or absence of 1 µM octreotide at different time points. Moreover, laser capture microdissected tumour cells and paraffin embedded tissue slides from SI-NETs at different stages of disease were used to identify transcriptional and translational expression. Microarrays analyses did not reveal relevant changes in SSTR expression levels. Unexpectedly, six novel genes were found to be upregulated by octreotide: annexin A1 (ANXA1), rho GTPase-activating protein 18 (ARHGAP18), epithelial membrane protein 1 (EMP1), growth/differentiation factor 15 (GDF15), TGF-beta type II receptor (TGFBR2) and tumour necrosis factor (ligand) superfamily member 15 (TNFSF15). Furthermore, these novel genes were expressed in tumour tissues at transcript and protein levels. We suggest that octreotide may use a potential novel framework to exert its beneficial effect as a drug and to convey its action on neuroendocrine cells. Thus, six novel genes may regulate cell growth and differentiation in normal and tumour neuroendocrine cells and have a role in a novel octreotide mechanism system. Octreotide is a widely used synthetic somatostatin analogue that significantly improves the management of neuroendocrine tumours (NETs). Octreotide acts through somatostatin receptors (SSTRs). However, the molecular mechanisms leading to successful disease control or symptom management, especially when SSTRs levels are low, are largely unknown. We provide novel insights into how octreotide controls NET cells. CNDT2.5 cells were treated from 1 day up to 16 months with octreotide and then were profiled using Affymetrix microarray analysis. Quantitative real-time PCR and western blot analyses were used to validate microarray profiling in silico data. WST-1 cell proliferation assay was applied to evaluate cell growth of CNDT2.5 cells in the presence or absence of 1 [micro]M octreotide at different time points. Moreover, laser capture microdissected tumour cells and paraffin embedded tissue slides from SI-NETs at different stages of disease were used to identify transcriptional and translational expression. Microarrays analyses did not reveal relevant changes in SSTR expression levels. Unexpectedly, six novel genes were found to be upregulated by octreotide: annexin A1 (ANXA1), rho GTPase-activating protein 18 (ARHGAP18), epithelial membrane protein 1 (EMP1), growth/differentiation factor 15 (GDF15), TGF-beta type II receptor (TGFBR2) and tumour necrosis factor (ligand) superfamily member 15 (TNFSF15). Furthermore, these novel genes were expressed in tumour tissues at transcript and protein levels. We suggest that octreotide may use a potential novel framework to exert its beneficial effect as a drug and to convey its action on neuroendocrine cells. Thus, six novel genes may regulate cell growth and differentiation in normal and tumour neuroendocrine cells and have a role in a novel octreotide mechanism system. Octreotide is a widely used synthetic somatostatin analogue that significantly improves the management of neuroendocrine tumours (NETs). Octreotide acts through somatostatin receptors (SSTRs). However, the molecular mechanisms leading to successful disease control or symptom management, especially when SSTRs levels are low, are largely unknown. We provide novel insights into how octreotide controls NET cells. CNDT2.5 cells were treated from 1 day up to 16 months with octreotide and then were profiled using Affymetrix microarray analysis. Quantitative real-time PCR and western blot analyses were used to validate microarray profiling in silico data. WST-1 cell proliferation assay was applied to evaluate cell growth of CNDT2.5 cells in the presence or absence of 1 μM octreotide at different time points. Moreover, laser capture microdissected tumour cells and paraffin embedded tissue slides from SI-NETs at different stages of disease were used to identify transcriptional and translational expression. Microarrays analyses did not reveal relevant changes in SSTR expression levels. Unexpectedly, six novel genes were found to be upregulated by octreotide: annexin A1 (ANXA1), rho GTPase-activating protein 18 (ARHGAP18), epithelial membrane protein 1 (EMP1), growth/differentiation factor 15 (GDF15), TGF-beta type II receptor (TGFBR2) and tumour necrosis factor (ligand) superfamily member 15 (TNFSF15). Furthermore, these novel genes were expressed in tumour tissues at transcript and protein levels. We suggest that octreotide may use a potential novel framework to exert its beneficial effect as a drug and to convey its action on neuroendocrine cells. Thus, six novel genes may regulate cell growth and differentiation in normal and tumour neuroendocrine cells and have a role in a novel octreotide mechanism system. Octreotide is a widely used synthetic somatostatin analogue that significantly improves the management of neuroendocrine tumours (NETs). Octreotide acts through somatostatin receptors ( SSTRs ). However, the molecular mechanisms leading to successful disease control or symptom management, especially when SSTRs levels are low, are largely unknown. We provide novel insights into how octreotide controls NET cells. CNDT2.5 cells were treated from 1 day up to 16 months with octreotide and then were profiled using Affymetrix microarray analysis. Quantitative real-time PCR and western blot analyses were used to validate microarray profiling in silico data. WST-1 cell proliferation assay was applied to evaluate cell growth of CNDT2.5 cells in the presence or absence of 1 µM octreotide at different time points. Moreover, laser capture microdissected tumour cells and paraffin embedded tissue slides from SI-NETs at different stages of disease were used to identify transcriptional and translational expression. Microarrays analyses did not reveal relevant changes in SSTR expression levels. Unexpectedly, six novel genes were found to be upregulated by octreotide: annexin A1 ( ANXA1 ), rho GTPase-activating protein 18 ( ARHGAP18 ), epithelial membrane protein 1 ( EMP1 ), growth/differentiation factor 15 ( GDF15 ), TGF-beta type II receptor ( TGFBR2 ) and tumour necrosis factor (ligand) superfamily member 15 ( TNFSF15 ). Furthermore, these novel genes were expressed in tumour tissues at transcript and protein levels. We suggest that octreotide may use a potential novel framework to exert its beneficial effect as a drug and to convey its action on neuroendocrine cells. Thus, six novel genes may regulate cell growth and differentiation in normal and tumour neuroendocrine cells and have a role in a novel octreotide mechanism system. Octreotide is a widely used synthetic somatostatin analogue that significantly improves the management of neuroendocrine tumours (NETs). Octreotide acts through somatostatin receptors (SSTRs). However, the molecular mechanisms leading to successful disease control or symptom management, especially when SSTRs levels are low, are largely unknown. We provide novel insights into how octreotide controls NET cells. CNDT2.5 cells were treated from 1 day up to 16 months with octreotide and then were profiled using Affymetrix microarray analysis. Quantitative real-time PCR and western blot analyses were used to validate microarray profiling in silico data. WST-1 cell proliferation assay was applied to evaluate cell growth of CNDT2.5 cells in the presence or absence of 1 µM octreotide at different time points. Moreover, laser capture microdissected tumour cells and paraffin embedded tissue slides from SI-NETs at different stages of disease were used to identify transcriptional and translational expression. Microarrays analyses did not reveal relevant changes in SSTR expression levels. Unexpectedly, six novel genes were found to be upregulated by octreotide: annexin A1 (ANXA1), rho GTPase-activating protein 18 (ARHGAP18), epithelial membrane protein 1 (EMP1), growth/differentiation factor 15 (GDF15), TGF-beta type II receptor (TGFBR2) and tumour necrosis factor (ligand) superfamily member 15 (TNFSF15). Furthermore, these novel genes were expressed in tumour tissues at transcript and protein levels. We suggest that octreotide may use a potential novel framework to exert its beneficial effect as a drug and to convey its action on neuroendocrine cells. Thus, six novel genes may regulate cell growth and differentiation in normal and tumour neuroendocrine cells and have a role in a novel octreotide mechanism system.Octreotide is a widely used synthetic somatostatin analogue that significantly improves the management of neuroendocrine tumours (NETs). Octreotide acts through somatostatin receptors (SSTRs). However, the molecular mechanisms leading to successful disease control or symptom management, especially when SSTRs levels are low, are largely unknown. We provide novel insights into how octreotide controls NET cells. CNDT2.5 cells were treated from 1 day up to 16 months with octreotide and then were profiled using Affymetrix microarray analysis. Quantitative real-time PCR and western blot analyses were used to validate microarray profiling in silico data. WST-1 cell proliferation assay was applied to evaluate cell growth of CNDT2.5 cells in the presence or absence of 1 µM octreotide at different time points. Moreover, laser capture microdissected tumour cells and paraffin embedded tissue slides from SI-NETs at different stages of disease were used to identify transcriptional and translational expression. Microarrays analyses did not reveal relevant changes in SSTR expression levels. Unexpectedly, six novel genes were found to be upregulated by octreotide: annexin A1 (ANXA1), rho GTPase-activating protein 18 (ARHGAP18), epithelial membrane protein 1 (EMP1), growth/differentiation factor 15 (GDF15), TGF-beta type II receptor (TGFBR2) and tumour necrosis factor (ligand) superfamily member 15 (TNFSF15). Furthermore, these novel genes were expressed in tumour tissues at transcript and protein levels. We suggest that octreotide may use a potential novel framework to exert its beneficial effect as a drug and to convey its action on neuroendocrine cells. Thus, six novel genes may regulate cell growth and differentiation in normal and tumour neuroendocrine cells and have a role in a novel octreotide mechanism system. |
| Audience | Academic |
| Author | Luque, Raúl M. Giandomenico, Valeria Cui, Tao Castaño, Justo P. Li, Su-Chen Öberg, Kjell Martijn, Cécile Essaghir, Ahmed Demoulin, Jean-Baptiste |
| AuthorAffiliation | University of Santiago de Compostela School of Medicine - CIMUS, Spain 5 Centre of Excellence for Endocrine Tumours, Uppsala University Hospital, Uppsala, Sweden 2 Department of Surgical Sciences, Anaesthesiology & Intensive Care, Science for Life Laboratory, Uppsala University, Uppsala, Sweden 1 Department of Medical Sciences, Endocrine Oncology, Science for Life Laboratory, Uppsala University, Uppsala, Sweden 3 Université Catholique de Louvain, de Duve Institute, Brussels, Belgium 4 Department of Cell Biology, Physiology, and Immunology, Instituto Maimónides de Investigación Biomédica (IMIBIC), Hospital Universitario Reina Sofia, University of Cordoba, and CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Cordoba, Spain |
| AuthorAffiliation_xml | – name: 3 Université Catholique de Louvain, de Duve Institute, Brussels, Belgium – name: 5 Centre of Excellence for Endocrine Tumours, Uppsala University Hospital, Uppsala, Sweden – name: 1 Department of Medical Sciences, Endocrine Oncology, Science for Life Laboratory, Uppsala University, Uppsala, Sweden – name: 2 Department of Surgical Sciences, Anaesthesiology & Intensive Care, Science for Life Laboratory, Uppsala University, Uppsala, Sweden – name: University of Santiago de Compostela School of Medicine - CIMUS, Spain – name: 4 Department of Cell Biology, Physiology, and Immunology, Instituto Maimónides de Investigación Biomédica (IMIBIC), Hospital Universitario Reina Sofia, University of Cordoba, and CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Cordoba, Spain |
| Author_xml | – sequence: 1 givenname: Su-Chen surname: Li fullname: Li, Su-Chen – sequence: 2 givenname: Cécile surname: Martijn fullname: Martijn, Cécile – sequence: 3 givenname: Tao surname: Cui fullname: Cui, Tao – sequence: 4 givenname: Ahmed surname: Essaghir fullname: Essaghir, Ahmed – sequence: 5 givenname: Raúl M. surname: Luque fullname: Luque, Raúl M. – sequence: 6 givenname: Jean-Baptiste surname: Demoulin fullname: Demoulin, Jean-Baptiste – sequence: 7 givenname: Justo P. surname: Castaño fullname: Castaño, Justo P. – sequence: 8 givenname: Kjell surname: Öberg fullname: Öberg, Kjell – sequence: 9 givenname: Valeria surname: Giandomenico fullname: Giandomenico, Valeria |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/23119007$$D View this record in MEDLINE/PubMed https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-186023$$DView record from Swedish Publication Index |
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| Copyright | COPYRIGHT 2012 Public Library of Science 2012 Li et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. 2012 Li et al 2012 Li et al |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Conceived and designed the experiments: SCL KÖ VG. Performed the experiments: SCL TC RML. Analyzed the data: SCL AE J-BD JPC KÖ VG. Contributed reagents/materials/analysis tools: SCL TC AE RML J-BD. Wrote the paper: SCL CM JPC VG. N/A. Competing Interests: The authors have declared that no competing interests exist. |
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| Snippet | Octreotide is a widely used synthetic somatostatin analogue that significantly improves the management of neuroendocrine tumours (NETs). Octreotide acts... |
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| SubjectTerms | Analysis Annexins Antineoplastic Agents - pharmacology Biology Biomarkers Cancer therapies Cell cycle Cell Differentiation - drug effects Cell growth Cell Line, Tumor Cell proliferation Cell Proliferation - drug effects Differentiation Disease control DNA microarrays Gene expression Genes Growth GTPase-activating protein Guanosine triphosphatases Hospitals Humans Immunology Intestinal Neoplasms - pathology Intestine, Small - pathology Laboratories Medicine Membrane proteins Metastasis Molecular modelling Neoplasm Staging Nets Neuroendocrine tumors Neuroendocrine Tumors - pathology Octreotide Octreotide - pharmacology Oncology Paraffin Physiology Proteins Receptors Receptors, Somatostatin - genetics RNA, Messenger - genetics RNA, Messenger - metabolism Science Signal Transduction - drug effects Small intestine Somatostatin Somatostatin - analogs & derivatives Somatostatin receptors Symptom management Tissues Transcription Transcription, Genetic - drug effects Transcriptome - drug effects Transforming growth factor-b Transforming growth factors Tumor necrosis factor Tumors Up-Regulation - drug effects |
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| Title | The Somatostatin Analogue Octreotide Inhibits Growth of Small Intestine Neuroendocrine Tumour Cells |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/23119007 https://www.proquest.com/docview/1326561660 https://www.proquest.com/docview/1126620935 https://pubmed.ncbi.nlm.nih.gov/PMC3485222 https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-186023 https://doaj.org/article/9793950de5904fd884b299674b0de96d http://dx.doi.org/10.1371/journal.pone.0048411 |
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