Microarray Analysis of Somatostatin Receptor 5‐Regulated Gene Expression Profiles in Murine Pancreas

Patel, Sanjeet G.; Zhou, Guisheng; Liu, Shi He; Li, Min; Jeong, Jae Wook; DeMayo, Francesco J.; Gingras, Marie Claude; Gibbs, Richard A.; Fisher, William E.; Brunicardi, F. Charles

doi:10.1007/s00268-008-9893-1

Cited by 8 publications

(5 citation statements)

References 86 publications

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“…SSTR5 is also involved in the regulation of angiogenesis (Zatelli et al, 2001) and apoptosis (Qiu et al, 2006; Wang et al, 2013). This is consistent with microarray studies of pancreatic RNA from SSTR5 −/− mice in which ablation of SSTR5 results in up-regulation of proliferated and angiogenic genes and suppression of apoptotic genes (Patel et al, 2009). …”

Section: Introductionsupporting

confidence: 88%

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Down-regulation of pancreatic and duodenal homeobox-1 by somatostatin receptor subtype 5: a novel mechanism for inhibition of cellular proliferation and insulin secretion by somatostatin

et al. 2014

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Somatostatin (SST) is a regulatory peptide and acts as an endogenous inhibitory regulator of the secretory and proliferative responses of target cells. SST’s actions are mediated by a family of seven transmembrane domain G protein-coupled receptors that comprise five distinct subtypes (SSTR1-5). SSTR5 is one of the major SSTRs in the islets of Langerhans. Homeodomain-containing transcription factor pancreatic and duodenal homeobox-1 (PDX-1) is essential for pancreatic development, β cell differentiation, maintenance of normal β cell functions in adults and tumorigenesis. Recent studies show that SSTR5 acts as a negative regulator for PDX-1 expression and that SSTR5 mediates somatostatin’s inhibitory effect on cell proliferation and insulin expression/excretion through down-regulating PDX-1 expression. SSTR5 exerts its inhibitory effect on PDX-1 expression at both the transcriptional level by down-regulating PDX-1 mRNA and the post-translational level by enhancing PDX-1 ubiquitination. Identification of PDX-1 as a transcriptional target for SSTR5 may help in guiding the choice of therapeutic cancer treatments.

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Section: Introductionsupporting

confidence: 88%

“…SSTR5 has been shown to regulate a specific set of genes linked to cell proliferation, apoptosis, angiogenesis, immunity and tumorigenesis (Patel et al, 2009). PDX-1 also regulates a group of genes related to cell proliferation, apoptosis, invasion and angiogenesis (Liu et al, 2011).…”

Section: Perspectivementioning

confidence: 99%

Down-regulation of pancreatic and duodenal homeobox-1 by somatostatin receptor subtype 5: a novel mechanism for inhibition of cellular proliferation and insulin secretion by somatostatin

et al. 2014

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“…12 A recent study may shed additional light on racial differences, discovering that somatostatin subtype receptor (SSTR5) is recognized as a regulator of pancreatic tissue and that genotype differences in SSTR5 may exist by race. 13–15 Studies have not adequately assessed the contribution of behavioral or genetic risk factors to racial differences in incidence.…”

Section: Resultsmentioning

confidence: 99%

Disparities in Pancreatic Cancer Treatment and Outcomes

Noel

Fiscella

2019

Health Equity

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Pancreatic cancer remains a major health concern; in the next 2 years, it will become the second leading cause of cancer deaths in the United States. Health disparities in the treatment of pancreatic cancer exist across many disciplines, including race and ethnicity, socioeconomic status (SES), and insurance. This narrative review discusses what is known about these disparities, with the goal of highlighting targets for equity promoting interventions. Methods: We performed a narrative review of health disparities in pancreatic cancer spanning greater than ten areas, including epidemiology, treatment, and outcome, using the PubMed NIH database from 2000 to 2019 in the Unites States. Results: African Americans (AAs) tend to present at diagnosis with later stage disease. AAs and Hispanics have lower rates of surgical resection, are more likely to be treated at low volume hospitals, and often experience higher rates of morbidity and mortality compared to white patients, although control for confounders is often limited. Insurance and SES also factor into the delivery of treatment for pancreatic cancer. Conclusion: Disparities by race and SES exist in the diagnosis and treatment of pancreatic cancer that are largely driven by race and SES. Improved understanding of underlying causes could inform interventions.

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“…It is not known whether somatostatin is also able to regulate its own expression, but there are some indications that this might be possible. The binding of somatostatin to SSTR5 mediates an inhibitory effect on islet cell survival and insulin expression [126,127]. Zhou et al [128] reported that SSTR5-induced signaling is linked to PDX1.…”

Section: Putative Autocrine Feedbackmentioning

confidence: 99%

Regulatory Mechanisms of Somatostatin Expression

Ampofo

Nalbach

Menger

et al. 2020

IJMS

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Somatostatin is a peptide hormone, which most commonly is produced by endocrine cells and the central nervous system. In mammals, somatostatin originates from pre-prosomatostatin and is processed to a shorter form, i.e., somatostatin-14, and a longer form, i.e., somatostatin-28. The two peptides repress growth hormone secretion and are involved in the regulation of glucagon and insulin synthesis in the pancreas. In recent years, the processing and secretion of somatostatin have been studied intensively. However, little attention has been paid to the regulatory mechanisms that control its expression. This review provides an up-to-date overview of these mechanisms. In particular, it focuses on the role of enhancers and silencers within the promoter region as well as on the binding of modulatory transcription factors to these elements. Moreover, it addresses extracellular factors, which trigger key signaling pathways, leading to an enhanced somatostatin expression in health and disease.

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Microarray Analysis of Somatostatin Receptor 5‐Regulated Gene Expression Profiles in Murine Pancreas

Cited by 8 publications

References 86 publications

Down-regulation of pancreatic and duodenal homeobox-1 by somatostatin receptor subtype 5: a novel mechanism for inhibition of cellular proliferation and insulin secretion by somatostatin

Down-regulation of pancreatic and duodenal homeobox-1 by somatostatin receptor subtype 5: a novel mechanism for inhibition of cellular proliferation and insulin secretion by somatostatin

Disparities in Pancreatic Cancer Treatment and Outcomes

Regulatory Mechanisms of Somatostatin Expression

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