ArticleOncogene2012
The new truncated somatostatin receptor variant sst5TMD4 is associated to poor prognosis in breast cancer and increases malignancy in MCF-7 cells.
Article in Oncogene, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 72 citations in OpenAlex.
- Trial
- An Integrative RNA Spliceosomic Landscape of Pancreatic Neuroendocrine Tumors Identifies Clinically Relevant Molecular Subgroups.Endocrine pathology · 2026Article
- Clinical value of circulating splicing factors in prostate cancer: SRRM1 as a novel predictive biomarker and therapeutic target.Molecular therapy. Oncology · 2024Article
- Altered CELF4 splicing factor enhances pancreatic neuroendocrine tumors aggressiveness influencing mTOR and everolimus response.Molecular therapy. Nucleic acids · 2024Article
- The uprise of RNA biology in neuroendocrine neoplasms: altered splicing and RNA species unveil translational opportunities.Reviews in endocrine & metabolic disorders · 2023Review
- CoQCellular oncology (Dordrecht, Netherlands) · 2023Article
- PRPF8 increases the aggressiveness of hepatocellular carcinoma by regulating FAK/AKT pathway via fibronectin 1 splicing.Experimental & molecular medicine · 2023Article
- Epigenetic and post-transcriptional regulation of somatostatin receptor subtype 5 (SSTMolecular oncology · 2022Article
- Somatostatin Receptor Splicing VariantInternational journal of molecular sciences · 2022Article
- Unleashing the Diagnostic, Prognostic and Therapeutic Potential of the Neuronostatin/GPR107 System in Prostate Cancer.Journal of clinical medicine · 2020Article
- Evaluation of Pan-SSTRs Targeted Radioligand [ACS medicinal chemistry letters · 2020Article
- Somatostatin Analogs in Clinical Practice: a Review.International journal of molecular sciences · 2020Review
- Dysregulation of the splicing machinery is directly associated to aggressiveness of prostate cancer.EBioMedicine · 2020Article
- Clinical Utility of Ghrelin-O-Acyltransferase (GOAT) Enzyme as a Diagnostic Tool and Potential Therapeutic Target in Prostate Cancer.Journal of clinical medicine · 2019Article
- Integrative genomics analysis of hub genes and their relationship with prognosis and signaling pathways in esophageal squamous cell carcinoma.Molecular medicine reports · 2019Article
- Splicing Machinery is Dysregulated in Pituitary Neuroendocrine Tumors and is Associated with Aggressiveness Features.Cancers · 2019Article
- Ghrelin-O-Acyltransferase (GOAT) Enzyme as a Novel Potential Biomarker in Gastroenteropancreatic Neuroendocrine Tumors.Clinical and translational gastroenterology · 2018Article
- International Union of Basic and Clinical Pharmacology. CV. Somatostatin Receptors: Structure, Function, Ligands, and New Nomenclature.Pharmacological reviews · 2018Review
- Molecular Genetic Studies of Pancreatic Neuroendocrine Tumors: New Therapeutic Approaches.Endocrinology and metabolism clinics of North America · 2018Review
- Clinical and functional implication of the components of somatostatin system in gastroenteropancreatic neuroendocrine tumors.Endocrine · 2018Article
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Authors and funding
11 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Somatostatin receptors (sst1-5) are present in different types of tumors, where they inhibit key cellular processes such as proliferation and invasion. Although ssts are densely expressed in breast cancer, especially sst2, their role and therapeutic potential remain uncertain. Recently, we identified a new truncated sst5 variant, sst5TMD4, which is related to the abnormal response of certain pituitary tumors to treatment with somatostatin analogs. Here, we investigated the possible role of sst5TMD4 in breast cancer. This study revealed that sst5TMD4 is absent in normal mammary gland, but is abundant in a subset of poorly differentiated human breast tumors, where its expression correlated to that of sst2. Moreover, in the MCF-7 breast cancer model cell, sst5TMD4 expression increased malignancy features such as invasion and proliferation abilities (both in cell cultures and nude mice). This was likely mediated by sst5TMD4-induced increase in phosphorylated extracellular signal-regulated kinases 1 and 2 and p-Akt levels, and cyclin D3 and Arp2/3 complex expression, which also led to mesenchymal-like phenotype. Interestingly, sst5TMD4 interacts physically with sst2 and thereby alters its signaling, enabling disruption of sst2 inhibitory feedback and providing a plausible basis for our findings. These results suggest that sst5TMD4 could be involved in the pathophysiology of certain types of breast tumors.
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