Characterization of somatostatin receptors (SSTRs) expression and antiproliferative effect of somatostatin analogues in aggressive thyroid cancers
Abstract
BACKGROUND: Certain human carcinomas have demonstrated a distinct expression of somatostatin receptors. Data on somatostatin receptor expression in follicular thyroid cancer and anaplastic thyroid cancer has been limited and conflicting. This study seeks to characterize somatostatin receptor expression in follicular thyroid cancer and anaplastic thyroid cancer and to assess the effects of somatostatin analogues.
METHODS: Anaplastic thyroid cancer (Hth7 and 8505C) and follicular thyroid cancer (FTC-236) (Sigma-Aldrich, St. Louis, MO) cells were cultured. Capillary immunoblotting and reverse transcription polymerase chain reaction (RT-PCR) were used to determine the basal expression of protein and mRNA of SSTR1-SSTR5. Cells were treated with the somatostatin analogues octreotide, pasireotride (SOM230), and KE-108 for 48h. IC50 was determined via 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay, and cell proliferation was measured by viable cell count. Presence of SSTR2 was assessed by immunohistochemistry.
RESULTS: Immunoblotting analysis demonstrated that most cell lines expressed SSTR1-SSTR3 and SSTR5 in varying degrees. Reverse transcription polymerase chain reaction analysis showed that mRNA expression for SSTR2 and SSTR3 correlated with protein expression. MTT assays showed that KE-108 and SOM230 were able to inhibit cell proliferation. Tissue microarray (TMA) showed that SSTR2 was highly expressed in human tissues of aggressive thyroid carcinomas.
CONCLUSION: Follicular thyroid cancer and anaplastic thyroid cancer express SSTR1-3 and SSTR5 in distinct fashions both at a message and protein level. Our results suggest that somatostatin receptors are still a relevant and promising drug target against non-medullary thyroid cancers.
The Di Bella's Method: Use of Somatostatin/Octreotide analogues and/or derivatives with pseudo-Metronomic Chemotherapy Cyclophosphamide and/or Hydroxyurea (together with others chemical compounds) in Head and Neck Cancer (the dosage and administration schedule must be individualised for each patient):
See also:
- Official Web Site: The Di Bella Method;
- Somatostatin in oncology, the overlooked evidences - In vitro, review and in vivo publications;
- Publication, 2018 Jul: Over-Expression of GH/GHR in Breast Cancer and Oncosuppressor Role of Somatostatin as a Physiological Inhibitor (from Di Bella's Foundation);
- Publication, 2019 Aug: The Entrapment of Somatostatin in a Lipid Formulation: Retarded Release and Free Radical Reactivity (from Di Bella's Foundation);
- Publication, 2019 Sep: Effects of Somatostatin and Vitamin C on the Fatty Acid Profile of Breast Cancer Cell Membranes (from Di Bella's Foundation);
- Publication, 2019 Sep: Effects of somatostatin, curcumin, and quercetin on the fatty acid profile of breast cancer cell membranes (from Di Bella's Foundation);
- Publication, 2020 Sep: Two neuroendocrine G protein-coupled receptor molecules, somatostatin and melatonin: Physiology of signal transduction and therapeutic perspectives (from Di Bella's Foundation);
The Di Bella's Method: Use of Prolactin Inhibitors Cabergoline and/or Bromocriptine, Somatostatin/Octreotide analogues and/or derivatives since 1977 associated with pseudo-Metronomic Chemotherapy Cyclophosphamide and/or Hydroxyurea - together with others chemical compounds - in several Oncological Pathologies:
- Pleural Mesothelioma: clinical records on 11 patients treated with Di Bella's Method;
- Malignant pleural mesothelioma, stage T3-T4. Consideration of a case study;
- Neuroblastoma: Complete objective response to biological treatment;
- Large B-cells Non-Hodgkin's Lymphoma, Stage IV-AE: a Case Report;
- Non-Hodgkin's Lymphoma, Stage III-B-E: a Case Report;
- Oesophageal squamocellular carcinoma: a complete and objective response;
- Pancreatic Adenocarcinoma: clinical records on 17 patients treated with Di Bella's Method;
- Complete objective response to biological therapy of plurifocal breast carcinoma;






