Somatostatin Receptors 3, 4 and 5 Play Important Roles in Gallbladder Cancer

Guo, Runsheng; Shi, Peidong; Zhou, Jingtao; Chen, Yueyu

doi:10.7314/apjcp.2013.14.7.4071

Cited by 11 publications

(13 citation statements)

References 37 publications

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“…Five-year survival rates for GBC patients are very low (Carriaga and Henson, 1995) and, at present, only surgical excision of all apparent malignancy is an effective treatment (Taner et al, 2004). Although several factors, such as cholelithiasis, heavy metals, hormone receptors and cell cycle regulators, are reported to play important roles in the development of GBC, the exact mechanisms of its genesis are not known and very little information is available on molecular events (Serra et al, 2002;Chhabra et al, 2012;Wu et al, 2012;Guo et al, 2013;Srivastava et al, 2013). The prevalence of GBC is significantly higher in certain countries such as Chile, Japan, India and Poland (Lazcano-Ponce et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

High Frequency of TP53 but not K-ras Gene Mutations in Bolivian Patients with Gallbladder Cancer

Asai

Loza²,

Roig³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Although genetic characteristics are considered to be a factor influencing the geographic variation in the prevalence of gallbladder cancer (GBC), they have not been well studied in Bolivia, which has a high prevalence rate of GBC. The purpose of this study was to examine the frequency of TP53 and K-ras mutations in Bolivian patients with GBC and to compare them with our previous data obtained in other high-GBC-prevalence countries, namely Japan, Chile, and Hungary. DNA was extracted from cancer sites in paraffin-embedded tissue from 36 patients using a microdissection technique. TP53 mutations at exons 5 to 8 and K-ras mutations at codons 12, 13 and 61 were examined using direct sequencing techniques. The data obtained were compared with those in the other high-GBC-prevalence countries. Of the 36 patients, 18 (50.0%) had a TP53 mutation (one mutation in each of 17 patients and three mutations in one patient), and only one (2.8%) had a K-ras mutation. Of the 20 TP53 mutations, 12 were of the transition type (60.0%). This rate was significantly lower than that in Chile (12/12, P<0.05). In addition, three mutations were of the CpG transition type (15.0%), which is a feature of endogenous mutation. All three were found in the hot spot region of the TP53 gene. In contrast, G:C to T:A transversion was found in Bolivia, suggesting the presence of exogenous carcinogens. Our findings suggest that the development of GBC in Bolivia is associated with both exogenous carcinogens and endogenous mechanisms. The identification of an environmental risk factor for GBC is needed to confirm these findings.

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Section: Introductionmentioning

confidence: 99%

High Frequency of TP53 but not K-ras Gene Mutations in Bolivian Patients with Gallbladder Cancer

Asai

Loza²,

Roig³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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“…SSTR5 knockout mice develop islet neoplasia associated with enlarged islets (Wang et al, 2004, 2005a,b). Due to its differential expression, SSTR5 is involved in tumorigenesis and drug responsiveness of a variety of human cancers including pancreatic cancer (Reubi et al, 1988; Li et al, 2011; Zhou et al, 2011a; Kaemmerer et al, 2013), pancreatic endocrine tumors (PETs) (Zhou et al, 2011b, 2012; Kaemmerer et al, 2013), pulmonary neuroendocrine tumors (Tsuta et al, 2012), gastroenteropancreatic neuroendocrine tumors (Kim et al, 2011a; Sclafani et al, 2011), small cell lung cancer (Oddstig et al, 2011), gallbladder cancer (Guo et al, 2013), colon cancer (Wang et al, 2013), endocrine pituitary tumors (Nishioka et al, 2011; Mayr et al, 2013; Chinezu et al, 2014), thyroid cancer (Ocak et al, 2013), corticotroph adenomas (Fleseriu and Petersenn, 2013), prostate cancer (Gu et al, 2010; Mazzucchelli et al, 2011; Lattanzio et al, 2013), and breast cancer (Gu et al, 2010). SSTR5 is also involved in the regulation of angiogenesis (Zatelli et al, 2001) and apoptosis (Qiu et al, 2006; Wang et al, 2013).…”

Section: Introductionmentioning

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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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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“…Shi et al reported that Sst promoter methylation is associated with decreased Sst protein expression in gastric cancer samples compared with normal gastric mucosa tissues [67]. Furthermore, Guo et al showed that Sst3 expression is lower in poorly differentiated gallbladder cancer compared to moderately and highly differentiated gallbladder cancer [68]. In the same study, it was shown that Sst4 expression is higher in gallbladder cancer with lymph node metastasis compared with tumours without lymph node metastasis [68].…”

Section: Cardiopulmonary Assessment In Primary Ciliary Dyskinesia [56mentioning

confidence: 96%

Research update for articles published in EJCI in 2012

Dullaart

Al-Daghri

Ashina

et al. 2014

Eur J Clin Investigation

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Somatostatin Receptors 3, 4 and 5 Play Important Roles in Gallbladder Cancer

Cited by 11 publications

References 37 publications

High Frequency of TP53 but not K-ras Gene Mutations in Bolivian Patients with Gallbladder Cancer

High Frequency of TP53 but not K-ras Gene Mutations in Bolivian Patients with Gallbladder Cancer

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

Research update for articles published in EJCI in 2012

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