scholarly journals Gene expression profiles and bioinformatics analysis of insulin‐like growth factor‐1 promotion of osteogenic differentiation

2019 ◽  
Vol 7 (10) ◽  
Author(s):  
Yashuai Yuan ◽  
Ruimeng Duan ◽  
Baolin Wu ◽  
Wei Huang ◽  
Xiuzhi Zhang ◽  
...  
2003 ◽  
Vol 15 (3) ◽  
pp. 228-235 ◽  
Author(s):  
Nicholas F. Paoni ◽  
Matthew W. Feldman ◽  
Linda S. Gutierrez ◽  
Victoria A. Ploplis ◽  
Francis J. Castellino

Mutations in the adenomatous polyposis coli (APC) gene that result in excessive β-catenin-induced cell signaling are implicated in the risk of colon cancer. Although the mechanism of APC-mediated tumorigenesis is known, the pathways that translate β-catenin signaling into tumor growth in vivo are undefined. To address this, gene expression profiles of normal intestinal epithelial cells were compared with those from adenomas and carcinomas from APCMin/+ mice, a model of APC-related colorectal cancer. The gene expression profiles of adenomas and carcinomas were very similar, which is consistent with the theory that carcinomas progress from adenomas in this model system. Tumors had altered transcript abundance for members of several pathways that influence cell growth and proliferation including growth factors/receptors, molecules involved in apoptosis, and protein processing and catabolism enzymes. Comparison of gene expression between adenomas and carcinomas revealed nine differentially expressed transcripts. These included members of three growth-regulating pathways, and the results are consistent with the increased growth potential of carcinomas. SRY-box containing gene 17 (Sox 17), a negative regulator of β-catenin signaling, and calbindin-D9K, a factor that enhances calcium transport, were more highly expressed in adenomas than carcinomas (∼4-fold and 15- to 22-fold, respectively). Transcript abundance for insulin-like growth factor binding protein 5, which mediates insulin-like growth factor function, was 2.6-fold greater in carcinomas. Because the changes in gene expression observed in this study are directly associated with a deficiency in APC, the data provide new insights into how loss of this important tumor suppressor translates into benign and malignant tumor growth.


2004 ◽  
Vol 11 (4) ◽  
pp. 897-911 ◽  
Author(s):  
G Eisenhofer ◽  
T-T Huynh ◽  
K Pacak ◽  
F M Brouwers ◽  
M M Walther ◽  
...  

Pheochromocytomas in von Hippel–Lindau (VHL) syndrome produce exclusively norepinephrine, whereas those in multiple endocrine neoplasia type 2 (MEN 2) produce epinephrine. This study examined the pathways activated in VHL-associated pheochromocytomas by comparing gene expression profiles in VHL and MEN 2 tumors in relationship to profiles in sporadic norepinephrine- and epinephrine-producing tumors. Larger and more distinct differences in gene expression among hereditary than sporadic tumors indicated the importance of the underlying mutation to gene expression profiles. Many of the genes over-expressed in VHL compared with MEN 2 tumors were clearly linked to the hypoxia-driven angiogenic pathways that are activated in VHL-associated tumorigenesis. Such genes included those for the glucose transporter, vascular endothelial growth factor (VEGF), placental growth factor, angiopoietin 2, tie-1, VEGF receptor 2 and its coreceptor, neuropilin-1. Other up-regulated genes, such as connective tissue growth factor, cysteine-rich 61, matrix metalloproteinase 1, vascular endothelial cadherin, tenascin C, stanniocalcin 1, and cyclooxygenases 1 and 2 are known to be involved in VEGF-regulated angiogenesis. Shared differences in expression of subsets of genes in norepinephrine- versus epinephrine-producing hereditary and sporadic pheochromocytomas indicated other differences in gene expression that may underlie the biochemical phenotype. Over-expression of the hypoxia-inducible transcription factor, HIF-2α, in norepinephrine-predominant sporadic and VHL tumors compared with epinephrine-producing tumors indicates that expression of this gene depends on the noradrenergic biochemical phenotype. The findings fit with the known expression of HIF-2α in norepinephrine-producing cells of the sympathetic nervous system and might explain both the development and noradrenergic biochemical phenotype of pheochromocytomas in VHL syndrome.


2019 ◽  
Vol 25 ◽  
pp. 9563-9571 ◽  
Author(s):  
Yingchun Hu ◽  
Lingxia Cheng ◽  
Wu Zhong ◽  
Muhu Chen ◽  
Qian Zhang

2020 ◽  
Author(s):  
Huatian Luo ◽  
Da-qiu Chen ◽  
Jing-jing Pan ◽  
Zhang-wei Wu ◽  
Can Yang ◽  
...  

Abstract Background: Pancreatic cancer has many pathologic types, among which pancreatic ductal adenocarcinoma (PDAC) is the most common one. Bioinformatics has become a very common tool for the selection of potentially pathogenic genes. Methods: Three data sets containing the gene expression profiles of PDAC were downloaded from the gene expression omnibus (GEO) database. The limma package of R language was utilized to explore the differentially expressed genes (DEGs). To analyze functions and signaling pathways, the Database Visualization and Integrated Discovery (DAVID) was used. To visualize the protein-protein interaction (PPI) of the DEGs ,Cytoscape was performed under the utilization of Search Tool for the Retrieval of Interacting Genes (STRING). With the usage of the plug-in cytoHubba in cytoscape software, the hub genes were found out. To verify the expression levels of hub genes, Gene Expression Profiling Interactive Analysis (GEPIA) was performed. Last but not least, UALCAN analysis online tool was implemented to analyze the overall survival. Results: The 376 DEGs were highly enriched in biological processes including signal transduction, apoptotic process and several pathways, mainly associated with Protein digestion and absorption and Pancreatic secretion pathway. The expression levels of nucleolar and spindle associated protein 1 (NUSAP1) and SHC binding and spindle associated 1 (SHCBP1) were discovered highly expressed in pancreatic ductal adenocarcinoma tissues. NUSAP1 and SHCBP1 had a high correlation with prognosis. Conclusions: The findings of this bioinformatics analysis indicate that NUSAP1 and SHCBP1 may be key factors in the prognosis and treatment of pancreatic cancer.


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