scholarly journals The role of the renin-angiotensin system in the appearance and progression of renal cell carcinoma: a literature review

2019 ◽  
Vol 15 (3) ◽  
pp. 143-149
Author(s):  
M. I. Kogan ◽  
Z. M. Akhokhov ◽  
E. A. Chernogubova ◽  
A. A. Gusev ◽  
Z. Kh. Oitova
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Molecular Mechanisms ◽  
Renin Angiotensin System ◽  
The Body ◽  
Molecular Medicine ◽  
Angiotensin System ◽  
Renin Angiotensin

Renal cell carcinoma (RCC) is one of the most common forms of malignant epithelial tumors of this localization. The development of new approaches to the diagnosis, prognosis and treatment of RCC is an topical issue of molecular medicine. The renin-angiotensin system (RAS) is not only an important component of the central and humoral mechanisms of controlling blood pressure and hydroelectrolytic balance, but also refers to the body systems involved in complex carcinogenesis pathways. Researches on the role of RAS in tumor progression are currently the priority. The data on the role of RAS in the development and progression of malignant tumors in the kidneys are being discussed. In this article, we present an overview of data on the role of RAS in the emergence and development of RCC, an analysis of the molecular mechanisms of development and progression of RCC, the prospects for using indicators of the RAS: angiotensin-converting enzymes (ACE), ACE2 and angiotensin II receptors as markers of diagnosis and monitoring of neoplastic transformation processes in the kidney. The prospects for the use of new, effective anticancer drugs with a targeted effect on definite indicators of the RAS of RCC were analyzed.

Renin-angiotensin system (RAS) blockade attenuates growth and metastatic potential of renal cell carcinoma in mice

2015 ◽  
Vol 33 (9) ◽  
pp. 389.e1-389.e7 ◽  
Author(s):  
Wedson F. Araújo ◽  
Marcelo A. Naves ◽  
Juliana N. Ravanini ◽  
Nestor Schor ◽  
Vicente P.C. Teixeira
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Renin Angiotensin System ◽  
Metastatic Potential ◽  
Angiotensin System ◽  
Renin Angiotensin

Prognostic Impact of Renin–Angiotensin System Blockade on Renal Cell Carcinoma After Surgery

2015 ◽  
Vol 22 (11) ◽  
pp. 3751-3759 ◽  
Author(s):  
Akira Miyajima ◽  
Satoshi Yazawa ◽  
Takeo Kosaka ◽  
Nobuyuki Tanaka ◽  
Suguru Shirotake ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Renin Angiotensin System ◽  
Prognostic Impact ◽  
Angiotensin System ◽  
Renin Angiotensin

scholarly journals Hypertension and angiotensin system inhibitors in patients with metastatic renal cell carcinoma

2016 ◽  
Author(s):  
Lisa Derosa ◽  
Hassane Izzedine ◽  
Laurence Albiges ◽  
Bernard Escudier
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Metastatic Renal Cell Carcinoma ◽  
Renal Cell ◽  
Angiotensin Receptor Blockers ◽  
Treatment Options ◽  
Renin Angiotensin System ◽  
Angiotensin Converting Enzyme Inhibitors ◽  
Converting Enzyme Inhibitors ◽  
Angiotensin System

Arterial hypertension (HTN) is a class effect of anti-vascular endothelial growth factor (VEGF) therapies, including the monoclonal antibody bevacizumab. Data are conflicting regarding the role of the renin-angiotensin system on angiogenesis and recent data suggest that the use of angiotensin system inhibitors (ASIs; angiotensin receptor blockers or angiotensin-converting enzyme inhibitors) is associated with improved survival in metastatic renal cell carcinoma (mRCC), particularly when used with VEGF targeted therapies. The aim of this review is to discuss the available treatment options for mRCC and associated incidence of hypertension as well as summarize the known data about ASIs use and mRCC. Additionally, given that the optimal management of HTN remains unclear, we will focus on prevention strategies and propose potential therapeutic approaches.

scholarly journals SETD2 deficiency impairs β-catenin destruction complex to facilitate renal cell carcinoma formation

2020 ◽  
Author(s):  
Hanyu Rao ◽  
Xiaoxue Li ◽  
Min Liu ◽  
Jing Liu ◽  
Wenxin Feng ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Molecular Mechanisms ◽  
Clear Cell ◽  
Set Domain ◽  
Cell Renal Cell Carcinoma ◽  
Incurable Disease ◽  
First Time

AbstractClear cell renal cell carcinoma (ccRCC) is a largely incurable disease that is highly relevant to epigenetic regulation including histone modification and DNA methylation. SET domain–containing 2 (SETD2) is a predominant histone methyltransferase catalyzing the trimethylation of histone H3 Lysine 36 (H3K36me3) and its mutations are highly relevant to clear cell renal cell carcinoma (ccRCC). However, its physiology role in ccRCC remains largely unexplored. Here we report that Setd2 deletion impairs the β-catenin destruction complex to facilitate ccRCC formation in a c-MYC-generated polycystic kidney disease (PKD) model, which can be relieved by an inhibitor of β-catenin-responsive transcription. Clinically, SETD2 loss is widely observed in ccRCC samples, and negatively correlated with expression of some members of β-catenin destruction complex, but positively correlated with the activation of Wnt/β-catenin signaling. Our findings thus highlight a previously unrecognized role of SETD2-mediated H3K36me3 modification in regulation of Wnt/β-catenin pathway in ccRCC.SummaryOur findings for the first time reveal a previously unrecognized role of the SETD2-mediated H3K36me3 modification in regulation of the Wnt/β-catenin pathway in ccRCC and shed light on the molecular mechanisms underlying the formation of renal cell carcinoma with epigenetic disorders.

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