Notch signaling pathway

elegans lin-12, informed by the first oncogenic mutation affecting a human Notch gene

SPON2 Is Upregulated through Notch Signaling Pathway and Promotes Tumor Progression in Gastric Cancer

SPON2 Is Upregulated through Notch Signaling Pathway and Promotes Tumor Progression in Gastric Cancer

Spondin-2 (SPON2) involved in cancer development and metastasis of many tumors; However, the role and the underlying mechanisms in gastric cancer is still unclear. In this study, we examined the role SPON2 and associated signaling pathway in gastric cancer progression and metastasis. SPON2 expression level was found to be regulated in gastric cancer cell lines and tissues of patients compared to gastric epithelial cells of normal and normal controls.

Furthermore, SPON2 silencing was observed to reduce cell proliferation and motility and reduce tumor growth in xenograft mice. Conversely, excess SPON2 found to increase cell proliferation and motility. Next, we focus on regulatory mechanisms SPON2 in gastric cancer. cDNA microarray and in vitro studies suggest that Notch signaling was significantly correlated with the expression SPON2.

Therefore, we confirm how Notch signaling pathway regulates the expression of Notch-related SPON2 using signaling interactions of transcription factors and reporter gene assay. In addition, activation of Notch signaling is observed to increase cell proliferation, migration, and invasion through SPON2 expression. Our study suggests that Notch signaling-mediated upregulation SPON2 associated with aggressive development of gastric cancer. In conclusion, we recommend SPON2 regulated by Notch signaling as a potential target gene to inhibit the development of gastric cancer.

SPON2 Is Upregulated through Notch Signaling Pathway and Promotes Tumor Progression in Gastric Cancer
SPON2 Is Upregulated through Notch Signaling Pathway and Promotes Tumor Progression in Gastric Cancer

PNO1, which negatively regulated by miR-340-5p, promoting the development of adenocarcinoma of the lung through the Notch signaling pathway

Many studies have shown that hyperactivation of ribosome biogenesis plays an important role in the initiation and progression of cancer. As the ribosome assembly factor, PNO1 play an important role in ribosome biogenesis. However, little is known about the expression and function in human tumors PNO1. In our study, we aimed to explore the functional role and molecular mechanisms that underlie PNO1 in human lung adenocarcinoma (LUAD). Both bioinformatics databases and tumor tissues showed that expression in tissues LUAD PNO1 higher than in the adjacent tissue and predicted poor survival in patients LUAD. In vitro and in vivo tests showed that downregulation of the expression of PNO1 suppressed cell proliferation and invasion LUAD. Further research found that miR-340-5p PNO1 depressed expression via direct binding to the 3 ‘translated region (UTR) of PNO1.

PNO1 expression negatively correlated with miR-340-5p LUAD expression in cells and tissue samples. Moreover, upregulation or downregulation of the expression of miR-340-5p reversed the inhibitory effects and excessive PNO1, respectively. Meanwhile, downregulation of Notch signaling pathway inhibits PNO1 modulated epithelial mesenchymal transition (EMT). These results indicate that PNO1, negatively regulated by miR-340-5p, plays an important role in the development of LUAD through the Notch signaling pathway. The miR-340-5p / PNO1 / Notch axis may be a potential target for the treatment of the individual and the right of patients LUAD in the future.
Forty Kunming mice were randomly divided into normal group (n = 10) and model group (n = 30).

Array Designer

AD6 1
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Nylon Array

MVSNGA110 10 Slides
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MVSNGA120 20 Slides
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Human Cell Array I

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Thiamphenicol Drug [HRP]

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Thiamphenicol Drug Residue [HRP]

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Human Drug Transporter I Primer Library

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Carboxyl Blue Particle Array Kit

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Carboxyl Blue Particle Array Kit

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Carboxyl Yellow Particle Array Kit

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Exo-Check Exosome Antibody Array

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UV Carboxyl Particle Array Kit

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HDAC Inhibitor Drug Screening Kit (Fluorometric)

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QPCR Kit RNA All Human E

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Model of ulcerative colitis induced by free drinking of 2% dextran sulfate sodium (DSS). After 15 days, rats were divided into model group, 6-gingerenol group and positive control group with 10 rats in each group. normal group and model group were treated with normal saline, 6-gingerenol group treated with 6-shogaol 100 mg / (kg · d), the positive control group treated with sulfasalazine 100 mg / (kg · d) for 20 days. Intestinal histopathological changes were observed, and the expression of Hes-1 and Mathematics-1protein in colonic epithelial cells was detected by double immunofluorescence labeling method.

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