Notch signaling in pancreatic endocrine cell and diabetes

Kim, Wook; Shin, Yu-Kyong; Kim, Byung-Joon; Egan, Josephine M.

doi:10.1016/j.bbrc.2009.12.115

Cited by 51 publications

(46 citation statements)

References 40 publications

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“…Luciferase reporter assay and rescue experiment confirmed that miR-613 targets 3′UTR of notch3 to suppress the expression of notch3 and inhibits pancreatic cancer proliferation. Notch 3 is a protein that in encoded by the NOTCH3 gene in human and is one of the important mediators in the Notch signaling pathway, which has been shown to maintain a pool of pancreatic progenitor cells at the early stage of pancreatic development, and governs pancreatic ductal cell differentiation [29]. Notch3 has been shown to be overexpressed in several types of cancers, which makes it a promising therapeutic target for cancer treatment [30].…”

Section: Discussionmentioning

confidence: 99%

LncRNA HOTAIR acts as competing endogenous RNA to control the expression of Notch3 via sponging miR-613 in pancreatic cancer

Cai

Yao

et al. 2017

Oncotarget

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Pancreatic cancer is one of the most deadly cancers with a poor prognosis. Though studies have implicated the roles of microRNAs in pancreatic cancer progression, little is known about the role of miR-613 in pancreatic cancer. In the present study, the expression of miR-613 was down-regulated in pancreatic cancer tissues and cancer cell lines. Down-regulation of miR-613 was positively correlated with tumor differentiation, advanced TNM stage, nodal metastasis and shorter overall survival in patients with pancreatic cancer. Overexpression of miR-613 suppressed cell proliferation, invasion and migration, and induced cell apoptosis and cell cycle arrest at G0/G1 phase in pancreatic cancer cells. Bioinformatics analysis, luciferase reporter assay and rescue experiments showed that notch3 was a direct target of miR-613. MiR-613 was inversely correlated with notch3 expression in pancreatic cancer tissues. The long non-coding RNA, HOX transcript antisense RNA (HOTAIR) was up-regulated in both pancreatic cancer tissues and cancer cell lines, and HOTAIR suppressed the expression of miR-613 via functioning as a competing endogenous RNA. In vivo studies showed that stable overexpression of miR-613 or knock-down of HOTAIR suppressed tumor growth and also reduced the expression of notch3. In conclusion, these results suggest that HOTAIR functions as a competing endogenous RNA to regulate notch3 expression via sponging miR-613 in pancreatic cancer.

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Section: Discussionmentioning

confidence: 99%

LncRNA HOTAIR acts as competing endogenous RNA to control the expression of Notch3 via sponging miR-613 in pancreatic cancer

Cai

Yao

et al. 2017

Oncotarget

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“…The fact that the inhibition of the hedgehog signals also leads to the ectopic appearance of the pancreatic structures in the organs such as the stomach and duodenum (45) indicates that this system also plays a role in determining the area in which the pancreas will develop. It has been shown that Notch signals stimulate exocrine cell differentiation, but suppress endocrine cell differentiation (46). Follistatin and FGF are also involved in the development of exocrine pancreatic progenitors (47).…”

Section: Pancreas Developmentmentioning

confidence: 99%

Development of Liver and Pancreas

Eşrefoğlu¹,

Taşlıdere²,

Çetin³

2016

Bezmialem Science

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The parenchyma of the liver and pancreas is derived from the endoderm, whereas the stroma is derived from the mesoderm. Both of them are derived from the endoderm of the foregut as the esophagus, stomach, and a part of duodenum. At the 3 rd -4 th of development, the liver, gallbladder and bile ducts become diverticulum hepaticum that is derived from the caudal portion of the foregut. There were inductive effects of septum transversum and cardiac mesoderm for the development of liver diverticulum. The pancreas arise from the endoderm of the foregut. The pancreas is derived from the fusion of the ventral and dorsal pancreas bulbs, which arise from the endoderm of the duodenum. The inductive effects of the notochord and dorsal aorta play a role in the development of the pancreas. In this manuscript, we attempted to review the morphological and functional development of the liver and pancreas with the aid of pictures obtained from various stages of prenatal and postnatal development in the organs of rats.

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“…Studies in mouse (reviewed by Kim et al, 2010) and fish (reviewed by Tiso et al, 2009) have implicated Notch signaling in regulating differentiation of pancreatic progenitors. We have previously identified a population of pancreatic Notch-responsive cells (PNCs) within the pancreatic duct ).…”

Section: Genetic Inducible Fate Mapping Of Notchresponsive Cells Of Tmentioning

confidence: 99%

Genetic inducible fate mapping in larval zebrafish reveals origins of adult insulin-producing β-cells

et al. 2011

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SUMMARYThe Notch-signaling pathway is known to be fundamental in controlling pancreas differentiation. We now report on using Crebased fate mapping to indelibly label pancreatic Notch-responsive cells (PNCs) at larval stages and follow their fate in the adult pancreas. We show that the PNCs represent a population of progenitors that can differentiate to multiple lineages, including adult ductal cells, centroacinar cells (CACs) and endocrine cells. These endocrine cells include the insulin-producing -cells. CACs are a functional component of the exocrine pancreas; however, our fate-mapping results indicate that CACs are more closely related to endocrine cells by lineage as they share a common progenitor. The majority of the exocrine pancreas consists of the secretory acinar cells; however, we only detect a very limited contribution of PNCs to acinar cells. To explain this observation we re-examined early events in pancreas formation. The pancreatic anlage that gives rise to the exocrine pancreas is located in the ventral gut endoderm (called the ventral bud). Ptf1a is a gene required for exocrine pancreas development and is first expressed as the ventral bud forms. We used transgenic marker lines to observe both the domain of cells expressing ptf1a and cells responding to Notch signaling. We do not detect any overlap in expression and demonstrate that the ventral bud consists of two cell populations: a ptf1-expressing domain and a Notch-responsive progenitor core. As pancreas organogenesis continues, the ventral bud derived PNCs align along the duct, remain multipotent and later in development differentiate to form secondary islets, ducts and CACs.

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Notch signaling in pancreatic endocrine cell and diabetes

Cited by 51 publications

References 40 publications

LncRNA HOTAIR acts as competing endogenous RNA to control the expression of Notch3 via sponging miR-613 in pancreatic cancer

LncRNA HOTAIR acts as competing endogenous RNA to control the expression of Notch3 via sponging miR-613 in pancreatic cancer

Development of Liver and Pancreas

Genetic inducible fate mapping in larval zebrafish reveals origins of adult insulin-producing β-cells

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