scholarly journals Alterations in Gene Expression of Renin-Angiotensin System Components and Related Proteins in Colorectal Cancer

2021 ◽  
Vol 2021 ◽  
pp. 1-17
Author(s):  
Danial Mehranfard ◽  
Gabriela Perez ◽  
Andres Rodriguez ◽  
Julia M. Ladna ◽  
Christopher T. Neagra ◽  
...  
Keyword(s):  
Gene Expression ◽  
Colorectal Cancer ◽  
Renin Angiotensin System ◽  
Gene Expression Omnibus ◽  
Data Repository ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Quantitative Expression ◽  
Genes Encoding ◽  
Thimet Oligopeptidase

Hypothesis/Introduction. Recent studies suggest involvement of the renin-angiotensin system (RAS) in cancers, including colorectal cancer (CRC). This study focuses on the association of genes encoding 17 proteins related to the RAS within a Japanese male CRC population. Materials and Methods. Quantitative expression of the RNA of these 17 genes in normal and cancerous tissues obtained using chip arrays from the public functional genomics data repository, Gene Expression Omnibus (GEO) application, was compared statistically. Results. Expression of four genes, AGT (angiotensinogen), ENPEP (aminopeptidase A) MME (neprilysin), and PREP (prolyl endopeptidase), was significantly upregulated in CRC specimens. Expression of REN (renin), THOP (thimet oligopeptidase), NLN (neurolysin), PRCP (prolyl carboxypeptidase), ANPEP (aminopeptidase N), and MAS1 (Mas receptor) was downregulated in CRC specimens. Conclusions. Presuming gene expression parallel protein expression, these results suggest that increased production of the angiotensinogen precursor of angiotensin (ANG) peptides, with the reduction of the enzymes that metabolize it to ANG II, can lead to accumulation of angiotensinogen in CRC tissues. Downregulation of THOP, NLN, PRCP, and MAS1 gene expression, whose proteins contribute to the ACE2/ANG 1-7/Mas axis, suggests that reduced activity of this RAS branch could be permissive for oncogenicity. Components of the RAS may be potential therapeutic targets for treatment of CRC.

scholarly journals Renin–angiotensin system gene polymorphisms and colorectal cancer risk: a meta-analysis

2019 ◽  
Vol 20 (4) ◽  
pp. 147032031988193
Author(s):  
Zhen Cheng ◽  
Zhiwei Liu
Keyword(s):  
Colorectal Cancer ◽  
Cancer Risk ◽  
Angiotensin Converting Enzyme ◽  
Meta Analysis ◽  
Renin Angiotensin System ◽  
Recessive Model ◽  
Colorectal Cancer Risk ◽  
Converting Enzyme ◽  
Angiotensin System ◽  
Renin Angiotensin

Objective: The renin–angiotensin system gene has been implicated in the progression of colorectal cancer. Nevertheless, the details of that role remain controversial. We performed a meta-analysis to investigate the correlation between renin–angiotensin system gene polymorphisms and colorectal cancer. Methods: We retrieved relevant studies from PubMed and Embase. Subsequently, fixed or random-effects models were used to calculate pooled odds ratios (ORs) with 95% confidence intervals (CIs). Results: We identified six studies of the angiotensin-converting enzyme insertion/deletion (I/D) polymorphism, and two studies of the angiotensinogen M235T polymorphism. The angiotensin-converting enzyme I/D polymorphism did not significantly correlate with colorectal cancer risk in the total population (DD vs. II: OR 0.77, 95% CI 0.39–1.50; DI vs. II: OR 1.05, 95% CI 0.85–1.30; dominant model: OR 0.94, 95% CI 0.68–1.31; recessive model: OR 1.01, 95% CI 0.80–1.27). Similarly, the angiotensinogen M235T polymorphism was not associated with colorectal cancer risk (TT vs. MM: OR 1.38, 95% CI 0.52–3.67; TM vs. MM: OR 1.19, 95% CI 0.96–1.47; dominant model: OR 1.28, 95% CI 0.77–2.14; recessive model: OR 1.17, 95% CI 0.53–2.59). Conclusion: Our findings suggest that the angiotensin-converting enzyme I/D and angiotensinogen M235T polymorphisms are unlikely to correlate with colorectal cancer.

scholarly journals Relationship between drugs affecting the renin-angiotensin system and colorectal cancer: The MCC-Spain study

2017 ◽  
Vol 99 ◽  
pp. 178-184 ◽  
Author(s):  
Trinidad Dierssen-Sotos ◽  
Inés Gómez-Acebo ◽  
Camilo Palazuelos ◽  
Francisco Rodriguez-Moranta ◽  
Beatriz Pérez-Gómez ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin

Regulation of nonclassical renin-angiotensin system receptor gene expression in the adrenal medulla by acute and repeated immobilization stress

2015 ◽  
Vol 308 (6) ◽  
pp. R517-R529 ◽  
Author(s):  
Regina Nostramo ◽  
Lidia Serova ◽  
Marcela Laukova ◽  
Andrej Tillinger ◽  
Chandana Peddu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adrenal Medulla ◽  
Immobilization Stress ◽  
Receptor Gene ◽  
Renin Angiotensin System ◽  
Mrna Levels ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Catecholamine Biosynthesis ◽  
Receptor Mrna

The involvement of the nonclassical renin-angiotensin system (RAS) in the adrenomedullary response to stress is unclear. Therefore, we examined basal and immobilization stress (IMO)-triggered changes in gene expression of the classical and nonclassical RAS receptors in the rat adrenal medulla, specifically the angiotensin II type 2 (AT2) and type 4 (AT4) receptors, (pro)renin receptor [(P)RR], and Mas receptor (MasR). All RAS receptors were identified, with AT2 receptor mRNA levels being the most abundant, followed by the (P)RR, AT1A receptor, AT4 receptor, and MasR. Following a single IMO, AT2 and AT4 receptor mRNA levels decreased by 90 and 50%, respectively. Their mRNA levels were also transiently decreased by repeated IMO. MasR mRNA levels displayed a 75% transient decrease as well. Conversely, (P)RR mRNA levels were increased by 50% following single or repeated IMO. Because of its abundance, the function of the (P)RR was explored in PC-12 cells. Prorenin activation of the (P)RR increased phosphorylation of extracellular signal-regulated kinase 1/2 and tyrosine hydroxylase at Ser31, likely increasing its enzymatic activity and catecholamine biosynthesis. Together, the broad and dynamic changes in gene expression of the nonclassical RAS receptors implicate their role in the intricate response of the adrenomedullary catecholaminergic system to stress.

scholarly journals 729-1 Modulation of Cardiac Hypertrophy by Blockade of the Renin Angiotensin System: Effects on LVH Regression, Gene Expression, and Survival

1995 ◽  
Vol 25 (2) ◽  
pp. 135A
Author(s):  
Heribert Schunkert ◽  
Günter Bruckschlegel ◽  
Stephan R. Holmer ◽  
Daniela Grimm ◽  
Eckhard P. Kromer ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cardiac Hypertrophy ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin

Albumin inhibits the insulin-mediated ACE2 increase in cultured podocytes

2014 ◽  
Vol 306 (11) ◽  
pp. F1327-F1334 ◽  
Author(s):  
Eva Márquez ◽  
Marta Riera ◽  
Julio Pascual ◽  
María José Soler
Keyword(s):  
Gene Expression ◽  
Angiotensin Ii ◽  
Real Time ◽  
Real Time Pcr ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Filtration Barrier ◽  
Gene And Protein Expression ◽  
Ace2 Gene

Podocytes are key cells in the glomerular filtration barrier with a major role in the development of diabetic nephropathy. Podocytes are insulin-sensitive cells and have a functionally active local renin-angiotensin system. The presence and activity of angiotensin-converting enzyme 2 (ACE2), the main role of which is cleaving profibrotic and proinflammatory angiotensin-II into angiotensin-(1–7), have been demonstrated in podocytes. Conditionally immortalized mouse podocytes were cultured with insulin in the presence and absence of albumin. We found that insulin increases ACE2 gene and protein expression, by real-time PCR and Western blotting, respectively, and enzymatic activity within the podocyte and these increases were maintained over time. Furthermore, insulin favored an “anti-angiotensin II” regarding ACE/ACE2 gene expression balance and decreased fibronectin gene expression as a marker of fibrosis in the podocytes, all studied by real-time PCR. Similarly, insulin incubation seemed to protect podocytes from cell death, studied by a terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling assay. However, all these effects disappeared in the presence of albumin, which may mimic albuminuria, a main feature of DN pathophysiology. Our results suggest that modulation of renin-angiotensin system balance, fibrosis, and apoptosis by insulin in the podocyte may be an important factor in preventing the development and progression of diabetic kidney disease, but the presence of albuminuria seems to block these beneficial effects.

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