scholarly journals Growth Factor-specific Signaling Pathway Stimulation and Gene Expression Mediated by ErbB Receptors

2001 ◽  
Vol 276 (25) ◽  
pp. 22685-22698 ◽  
Author(s):  
Colleen Sweeney ◽  
Douglas Fambrough ◽  
Christine Huard ◽  
A. John Diamonti ◽  
Eric S. Lander ◽  
...  
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Signaling Pathway ◽  
Erbb Receptors ◽  
Specific Signaling Pathway

scholarly journals An FF Domain-Dependent Protein Interaction Mediates a Signaling Pathway for Growth Factor-Induced Gene Expression

2005 ◽  
Vol 17 (1) ◽  
pp. 23-35 ◽  
Author(s):  
Wei Jiang ◽  
Raffaella Sordella ◽  
Guang-Chao Chen ◽  
Shweta Hakre ◽  
Ananda L. Roy ◽  
...  
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Signaling Pathway ◽  
Protein Interaction ◽  
Dependent Protein

scholarly journals Identification of Immune-Related Risk Signatures for the Prognostic Prediction in Oral Squamous Cell Carcinoma

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Chen Zou ◽  
Dahong Huang ◽  
Haigang Wei ◽  
Siyuan Wu ◽  
Jing Song ◽  
...  
Keyword(s):  
Gene Expression ◽  
Squamous Cell Carcinoma ◽  
Growth Factor ◽  
Oral Squamous Cell Carcinoma ◽  
Signaling Pathway ◽  
Immune Cell ◽  
Risk Group ◽  
Growth Factor Receptor ◽  
Immune Cell Infiltration ◽  
Related Risk

Background. Oral squamous cell carcinoma (OSCC) is the most common type of oral cancer, which remains a major cause of morbidity and mortality in patients with head and neck cancers. However, the critical immune-related signatures and their prognostic values have rarely been investigated. Materials and Methods. Gene differential analysis was used to measure the differences of gene expression between the groups. Correlation analysis was used to assess the association between the gene expression levels and immune-related risk score/DNA methylation levels. The gene set enrichment analysis (GSEA) was used to identify the pathways or cell types enriched by those identified differentially expressed genes (DEGs). Results. In this study, we identified four immune-related gene signatures, including CTSG, TNFRSF4, LCORL, and PLAU, that were significantly associated with the overall survival in OSCC patients from the Cancer Genome Atlas (TCGA) OSCC cohort. Moreover, these four immune-related signatures were differentially expressed between the OSCC and nontumor tissues. The two groups (high and low risk) stratified by the immune-related risk scores had significantly different OS and mortality rates. The gene expression patterns and prognostic values of these immune-related signatures were also verified in two independent validation cohorts. Furthermore, the downregulated genes in the high-risk group (which were also upregulated in the low-risk group) were significantly enriched in the cell type-specific signatures of type 2 T helper cell (Th2), plasmacytoid dendritic cell (pDC), and memory B cell. In contrast, the upregulated genes in the high-score group were enriched in growth factor receptor-related signaling pathways, such as the VEGFA-VEGFR2 signaling pathway, PI3K-Akt signaling pathway, focal adhesion-PI3K-Akt-mTOR signaling pathway, and PDGF pathway, suggesting that those pathways were inversely correlated with immune cell infiltration. Conclusion. In summary, the immune-related signatures had the potential for predicting the risk of OSCC patients. Moreover, the present study also improved our understanding of the association between the growth factor receptor pathways and immune cell infiltration in OSCC.

scholarly journals WNT signaling is required for peritoneal membrane angiogenesis

2018 ◽  
Vol 314 (6) ◽  
pp. F1036-F1045 ◽  
Author(s):  
Manreet Padwal ◽  
Genyang Cheng ◽  
Limin Liu ◽  
Felix Boivin ◽  
Azim S. Gangji ◽  
...  
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Wnt Signaling ◽  
Solute Transport ◽  
Signaling Pathway ◽  
Wnt Signaling Pathway ◽  
Peritoneal Membrane ◽  
Peritoneal Fibrosis ◽  
Membrane Injury ◽  
Mesenchymal Transition

The wingless-type mouse mammary tumor virus integration site family (WNT) signaling pathway is involved in wound healing and fibrosis. We evaluated the WNT signaling pathway in peritoneal membrane injury. We assessed WNT1 protein expression in the peritoneal effluents of 54 stable peritoneal dialysis (PD) patients and WNT-related gene expression in ex vivo mesothelial cell cultures from 21 PD patients. In a transforming growth factor-β (TGF-β)-mediated animal model of peritoneal fibrosis, we evaluated regulation of the WNT pathway and the effect of WNT inhibition on peritoneal fibrosis and angiogenesis. WNT1 and WNT2 gene expression were positively correlated with peritoneal membrane solute transport in PD patients. In the mouse peritoneum, TGF-β-induced peritoneal fibrosis was associated with increased expression of WNT2 and WNT4. Peritoneal β-catenin protein was significantly upregulated after infection with adenovirus expressing TGF-β (AdTGF-β) along with elements of the WNT signaling pathway. Treatment with a β-catenin inhibitor (ICG-001) in mice with AdTGF-β-induced peritoneal fibrosis resulted in attenuation of peritoneal angiogenesis and reduced vascular endothelial growth factor. Similar results were also observed with the WNT antagonist Dickkopf-related protein (DKK)-1. In addition to this, DKK-1 blocked epithelial-mesenchymal transition and increased levels of the cell adhesion protein E-cadherin. We provide evidence that WNT signaling is active in the setting of experimental peritoneal fibrosis and WNT1 correlates with patient peritoneal membrane solute transport in PD patients. Intervention in this pathway is a possible therapy for peritoneal membrane injury.

scholarly journals Exercise-induced modification of the skeletal muscle transcriptome in Arabian horses

2017 ◽  
Vol 49 (6) ◽  
pp. 318-326 ◽  
Author(s):  
Katarzyna Ropka-Molik ◽  
Monika Stefaniuk-Szmukier ◽  
Kacper Z˙ukowski ◽  
Katarzyna Piórkowska ◽  
Monika Bugno-Poniewierska
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Vascular Endothelial Growth Factor ◽  
Fatty Acid ◽  
Growth Factor ◽  
Calcium Signaling ◽  
Signaling Pathway ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor ◽  
Skeletal Muscle Transcriptome

It has been found that Arabian and Thoroughbred horses differ in muscle fiber structure and thus in physiological changes occurring in muscles during exercise. The aim of the present study was to identify the global gene expression modifications that occur in skeletal muscle following a training regime to prepare for flat racing. Whole transcriptomes of muscle (gluteus medius) were compared between three time points of tissue collection: T0 (untrained horses), T1 (horses after intense gallop phase), and T2 (horses at the end of racing season), 23 samples in total. The numerous groups of exercise-regulated differentially expressed genes (DEGs) were related to muscle cell structure and signaling and included insulin-like growth factor 1 receptor ( IGF1R), insulin receptor ( INSR), transforming growth factor beta receptors 1 and 2 ( TGFBR1, TGFBR2), vascular endothelial growth factor B ( VEGFB); epidermal growth factor ( EGF), hepatocyte growth factor ( HGF), and vascular endothelial growth factor D ( FIGF). In Arabian horses, exercise modified the expression of genes belonging to the PPAR signaling pathway (e.g., PPARA, PPARD, and PLIN2), calcium signaling pathway, and pathways associated with metabolic processes (e.g., oxidative phosphorylation, fatty acid metabolism, glycolysis/gluconeogenesis, and citrate cycle). According to detected gene expression modifications, our results suggested that in Arabian horses, exercise switches energy generation toward fatty acid utilization and enhances glycogen transport and calcium signaling. The use of the RNA-Seq approach in analyzing the skeletal muscle transcriptome allowed for the proposal of a panel of new candidate genes potentially related to body homeostasis maintenance and racing performance in Arabian horses.

scholarly journals Identification of the possible therapeutic targets in the insulin-like growth factor 1 receptor pathway in a cohort of Egyptian hepatocellular carcinoma complicating chronic hepatitis C type 4

2020 ◽  
Vol 14 (1) ◽  
pp. 1-11
Author(s):  
Nada M.K. Mabrouk ◽  
Dalal M. Elkaffash ◽  
Mona Abdel-Hadi ◽  
Salah-ElDin Abdelmoneim ◽  
Sameh Saad ElDeen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Hepatocellular Carcinoma ◽  
Hepatitis C ◽  
Growth Factor ◽  
Signaling Pathway ◽  
Pathway Analysis ◽  
Expression Patterns ◽  
Gene Expression Patterns ◽  
Insulin Like Growth Factor ◽  
Tumor Characteristics

Background: Molecular targeted drugs are the first line of treatment of advanced hepatocellular carcinoma (HCC) due to its chemo- and radioresistant nature. HCC has several well-documented etiologic factors that drive hepatocarcinogenesis through different molecular pathways. Currently, hepatitis C virus (HCV) is a leading cause of HCC. Therefore, we included a unified cohort of HCV genotype 4-related HCCs to study the expression levels of genes involved in the insulin-like growth factor 1 receptor (IGF1R) pathway, which is known to be involved in all aspects of cancer growth and progression. Aim: Determine the gene expression patterns of IGF1R pathway genes in a cohort of Egyptian HCV-related HCCs. Correlate them with different patient/tumor characteristics. Determine the activity status of involved pathways. Methods: Total ribonucleic acid (RNA) was extracted from 32 formalin-fixed paraffin-embedded tissues of human HCV-related HCCs and 6 healthy liver donors as controls. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) using RT2 Profiler PCR Array for Human Insulin Signaling Pathway was done to determine significantly up- and downregulated genes with identification of most frequently coregulated genes, followed by correlation of gene expression with different patient/tumor characteristics. Finally, canonical pathway analysis was performed using the Ingenuity Pathway Analysis software. Results: Six genes – AEBP1, AKT2, C-FOS, PIK3R1, PRKCI, SHC1 – were significantly overexpressed. Thirteen genes – ADRB3, CEBPA, DUSP14, ERCC1, FRS3, IGF2, INS, IRS1, JUN, MTOR, PIK3R2, PPP1CA, RPS6KA1 – were significantly underexpressed. Several differentially expressed genes were related to different tumor/patient characteristics. Nitric oxide and reactive oxygen species production pathway was significantly activated in the present cohort, while the growth hormone signaling pathway was inactive. Conclusions: The gene expression patterns identified in this study may serve as possible therapeutic targets in HCV-related HCCs. The most frequently coregulated genes may serve to guide combined molecular targeted therapies. The IGF1R pathway showed evidence of inactivity in the present cohort of HCV-related HCCs, so targeting this pathway in therapy may not be effective.

scholarly journals Dexamethasone-induced intrauterine growth restriction impacts the placental prolactin family, insulin-like growth factor-II and the Akt signaling pathway

2005 ◽  
Vol 185 (2) ◽  
pp. 253-263 ◽  
Author(s):  
Rupasri Ain ◽  
Lindsey N Canham ◽  
Michael J Soares
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Signaling Pathway ◽  
Intrauterine Growth Restriction ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Placental Development ◽  
Junctional Zone ◽  
Intrauterine Growth ◽  
Factor Ii

Intrauterine growth restriction (IUGR) is a major cause of perinatal death and neonatal morbidity and mortality. There are numerous causes of IUGR. Glucocorticoid-induced IUGR is highly relevant because administration of synthetic glucocorticoids, principally dexamethasone, to women threatened by premature labor is widely used in clinical practice. Fetal growth is directly related to placental growth and development. In this report, we analyzed the effect of dexamethasone on placental development in the rat. Dexamethasone administered between days 13 and 20 of pregnancy not only induced IUGR but also decreased placental mass by approximately 50%. Impaired placental development was associated with dysregulated placental prolactin (PRL) family and insulin-like growth factor-II (IGF-II) gene expression. Furthermore, there was a significant decrease in the activation of Akt/protein kinase B in the junctional zone of the placenta, as assessed by the phosphorylation status of Akt and the pro-apoptotic protein BAD, a downstream target of the Akt signaling pathway. Such changes are consistent with increases in indices of apoptosis, including increased cleavage of poly(ADP-ribose) polymerase (PARP) in the junctional zone of the placenta of dexamethasone-treated rats. In summary, dexamethasone-induced IUGR is associated with placental insufficiency, including dysregulated placental hormone/cytokine gene expression and down-regulation of the IGF-II/Akt signaling pathway resulting in increases in indices of placental apoptosis.

Fibroblast growth factor 23 impairs phosphorus and vitamin D metabolism in vivo and suppresses 25-hydroxyvitamin D-1α-hydroxylase expression in vitro

2007 ◽  
Vol 293 (5) ◽  
pp. F1577-F1583 ◽  
Author(s):  
Farzana Perwad ◽  
Martin Y. H. Zhang ◽  
Harriet S. Tenenhouse ◽  
Anthony A. Portale
Keyword(s):  
Gene Expression ◽  
Vitamin D ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Signaling Pathway ◽  
Fibroblast Growth Factor 23 ◽  
Fibroblast Growth ◽  
Vitamin D Metabolism ◽  
Fgf 23 ◽  
Dose Dependent

Fibroblast growth factor-23 (FGF-23) is critical to the pathogenesis of a distinct group of renal phosphate wasting disorders: tumor-induced osteomalacia, X-linked hypophosphatemia, and autosomal dominant and autosomal recessive hypophosphatemic rickets. Excess circulating FGF-23 is responsible for their major phenotypic features which include hypophosphatemia due to renal phosphate wasting and inappropriately low serum 1,25(OH)2D concentrations. To characterize the effects of FGF-23 on renal sodium-phosphate (Na/Pi) cotransport and vitamin D metabolism, we administered FGF-23(R176Q) to normal mice. A single injection (0.33 μg/g body wt) induced significant hypophosphatemia, 20 and 29% decreases ( P < 0.001) in brush-border membrane (BBM) Na/Pi cotransport at 5 and 17 h after injection, respectively, and comparable decreases in the abundance of type IIa Na/Pi cotransporter protein in BBM. Multiple injections (6, 12, and 24 μg/day for 4 days) induced dose-dependent decreases (38, 63, and 75%, respectively) in renal abundance of 1α-hydroxylase mRNA ( P < 0.05). To determine whether FGF-23(R176Q) exerts a direct action on 1α-hydroxylase gene expression, we examined its effects in cultured human (HKC-8) and mouse (MCT) renal proximal tubule cells. FGF-23(R176Q) (1 to 10 ng/ml) induced a dose-dependent decrease in 1α-hydroxylase mRNA with a maximum suppression of 37% ( P < 0.05). Suppression was detectable after 6 h of exposure and maximal after 21 h. In MCT cells, FGF-23(R176Q) suppressed 1α-hydroxylase mRNA and activated the ERK1/2 signaling pathway. The MAPK inhibitor PD98059 effectively abolished FGF-23-induced suppression of 1α-hydroxylase mRNA by blocking signal transduction via ERK1/2. These novel findings provide evidence that FGF-23 directly regulates renal 1α-hydroxylase gene expression via activation of the ERK1/2 signaling pathway.

Experimental diabetes increases insulinlike growth factor I and II receptor concentration and gene expression in kidney

Diabetes ◽  
1990 ◽  
Vol 39 (12) ◽  
pp. 1490-1497 ◽  
Author(s):  
H. Werner ◽  
Z. Shen-Orr ◽  
B. Stannard ◽  
B. Burguera ◽  
C. T. Roberts ◽  
...  
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Experimental Diabetes ◽  
Factor I ◽  
Insulinlike Growth Factor ◽  
Receptor Concentration ◽  
Growth Factor I ◽  
Insulinlike Growth Factor I
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