scholarly journals Circulating biomarkers in renal cell carcinoma: the link between microRNAs and extracellular vesicles, where are we now?

2014 ◽  
Vol 1 (8) ◽  
pp. 84-98 ◽  
Author(s):  
Ana L Teixeira ◽  
Francisca Dias ◽  
Mónica Gomes ◽  
Mara Fernandes ◽  
Rui Medeiros
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Genetic Material ◽  
Tumor Development ◽  
Cell Communication ◽  
Bioactive Molecules ◽  
Screening Tests ◽  
Transcriptional Level ◽  
Incidence And Mortality

Renal cell carcinoma (RCC) is a lethal urological cancer, with incidence and mortality rates increasing by 2-3% per decade. The lack of   standard screening tests contributes to the fact that one-third of patients are diagnosed with locally invasive or metastatic disease. Moreover, 20-40% of RCC patients submitted to surgical nephrectomy will develop metastasis. MicroRNAs (miRNAs) are small non-coding RNAs responsible for gene regulation at a post-transcriptional level.  It is accepted that they are deregulated in cancer and can influence tumor development. Thus, miRNAs are promising RCC biomarkers, since they can be detected using non-invasive methods. They are highly stable and easier to quantify in circulating biofluids. The elevated miRNA stability in circulating samples may be the consequence of their capacity to circulate inside of extracellular microvesicles (EMVs), for example, the exosomes.  The EMVs are bilayered membrane vesicles secreted by all cell types. They can be released in the interstitial space or into circulating biofluids, which allows the travelling, binding and entrance of these vesicles in receptor cells. This type of cell communication can shuttle bioactive molecules between cells, allowing the horizontal transference of genetic material. In this review, we focus on circulating miRNAs (miR-210, miR-1233, miR-221, miR-15a, miR-451, miR-508, miR-378) in the biofluids of RCC patients and attempt to establish the diagnostic and prognostic accuracy, their synergic effects, and the pathways involved in RCC biology.

AN INTERLEUKIN-10 PROMOTER POLYMORPHISM MAY INFLUENCE TUMOR DEVELOPMENT IN RENAL CELL CARCINOMA

2005 ◽  
Vol 173 (3) ◽  
pp. 709-712 ◽  
Author(s):  
E. HAVRANEK ◽  
W.M. HOWELL ◽  
H.M. FUSSELL ◽  
J.A. WHELAN ◽  
M.A. WHELAN ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Tumor Development ◽  
Interleukin 10 ◽  
Promoter Polymorphism

scholarly journals A 17-Gene Signature Predicted Prognosis in Renal Cell Carcinoma

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Fan Li ◽  
Weifeng Hu ◽  
Wei Zhang ◽  
Guohao Li ◽  
Yonglian Guo
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Malignant Tumors ◽  
Prognostic Significance ◽  
Gene Signature ◽  
The Cancer Genome Atlas ◽  
Prognostic Indicators ◽  
Incidence And Mortality ◽  
Tcga Dataset

Renal cell carcinoma (RCC), which was one of the most common malignant tumors in urinary system, had gradually increased incidence and mortality in recent years. Although significant advances had been made in molecular and biology research on the pathogenesis of RCC, effective treatments and prognostic indicators were still lacking. In order to predict the prognosis of RCC better, we identified 17 genes that were associated with the overall survival (OS) of RCC patients from The Cancer Genome Atlas (TCGA) dataset and a 17-gene signature was developed. Through SurvExpress, we analyzed the expression differences of the 17 genes and their correlation with the survival of RCC patients in five datasets (ZHAO, TCGA, KIPAN, KIRC, and KIRP), and then evaluated the survival prognostic significance of the 17-gene signature for RCC. Our results showed that the 17-gene signature had a predictive prognostic value not only in single pathologic RCC, but also in multiple pathologic types of RCC. In conclusion, the 17-gene signature model was related to the survival of RCC patients and could help predict the prognosis with significant clinical implications.

scholarly journals Renal Cell Carcinoma – How Can We Predict its Outcomes in Clinical Practice?

2013 ◽  
Vol 13 (1) ◽  
pp. 63-70
Author(s):  
Ieva Vaivode ◽  
Vilnis Lietuvietis ◽  
Alinta Hegmane ◽  
Iveta Kudaba
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Predictive Accuracy ◽  
Treatment Strategies ◽  
Simple Algorithm ◽  
Mortality Data ◽  
Routine Practice ◽  
Clinical Scenarios ◽  
Incidence And Mortality

Summary Morbidity and mortality data of RCC (renal cell carcinoma) differs a lot among the European countries. In Latvia a growing trend in both incidence and mortality rates is still observed. The expanding availability of multiple treatment strategies has increased the importance of skilled individualized outcome prediction for patients. Several prognostic factors are available in RCC including anatomical, histological, clinical and molecular ones, but none of them is very precise, when used alone. Therefore increasing number of prognostic systems has been created in local and metastatic disease to increase predictive accuracy. In order to encourage the clinicians to use the available models in their routine practice, we tried to select the most relevant ones and include them in a simple algorithm to be used in common clinical scenarios throughout entire history of the disease in patients with RCC

scholarly journals Intra-tumor heterogeneity and clonal exclusivity in renal cell carcinoma

2018 ◽  
Author(s):  
Ariane L. Moore ◽  
Jack Kuipers ◽  
Jochen Singer ◽  
Elodie Burcklen ◽  
Peter Schraml ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Tumor Heterogeneity ◽  
Tumor Development ◽  
Treatment Strategies ◽  
Evolutionary Process ◽  
Tumor Evolution ◽  
Cell Renal Cell Carcinoma ◽  
Gene Pairs

AbstractTumorigenesis is an evolutionary process in which different clones evolve over time. Interactions between clones can affect tumor evolution and hence disease progression and treatment outcome. We analyzed 178 tumor samples in 89 clear cell renal cell carcinoma patients and found high intra-tumor heterogeneity with 62% of mutations detected in only one of two biopsies per patient. We developed a novel statistical test to identify gene pairs that are altered in co-occurring clones of the same tumor, including the pairsTP53andMUC16, as well asBAP1andTP53. The mutations in these gene pairs are clonally exclusive meaning that they occurred in different branches of the tumor phylogeny, suggesting a synergistic effect between the two clones carrying these mutations. Our analysis sheds new light on tumor development and implies that clonal interactions are common within tumors, which may eventually open up novel treatment strategies to improve cancer treatment.

scholarly journals HMGCR inhibition stabilizes the glycolytic enzyme PKM2 to support the growth of renal cell carcinoma

PLoS Biology ◽  
2021 ◽  
Vol 19 (4) ◽  
pp. e3001197
Author(s):  
Jiajun Huang ◽  
Xiaoyu Zhao ◽  
Xiang Li ◽  
Jiwei Peng ◽  
Weihao Yang ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Tumor Development ◽  
Serum Levels ◽  
Glycolytic Enzyme ◽  
Hsp90 Expression ◽  
Cholesterol Biosynthetic Pathway ◽  
Underlying Mechanisms ◽  
Rate Limiting

Renal cell carcinoma (RCC) is responsible for most cases of the kidney cancer. Previous research showed that low serum levels of cholesterol level positively correlate with poorer RCC-specific survival outcomes. However, the underlying mechanisms and functional significance of the role of cholesterol in the development of RCC remain obscure. 3-Hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR) plays a pivotal role in RCC development as it is the key rate-limiting enzyme of the cholesterol biosynthetic pathway. In this study, we demonstrated that the inhibition of HMGCR could accelerate the development of RCC tumors by lactate accumulation and angiogenesis in animal models. We identified that the inhibition of HMGCR led to an increase in glycolysis via the regulated HSP90 expression levels, thus maintaining the levels of a glycolysis rate-limiting enzyme, pyruvate kinase M2 (PKM2). Based on these findings, we reversed the HMGCR inhibition-induced tumor growth acceleration in RCC xenograft mice by suppressing glycolysis. Furthermore, the coadministration of Shikonin, a potent PKM2 inhibitor, reverted the tumor development induced by the HMGCR signaling pathway.

scholarly journals Increased nuclear factor-κB activation is related to the tumor development of renal cell carcinoma

2003 ◽  
Vol 24 (3) ◽  
pp. 377-384 ◽  
Author(s):  
Mototsugu Oya ◽  
Atsushi Takayanagi ◽  
Akio Horiguchi ◽  
Ryuichi Mizuno ◽  
Masafumi Ohtsubo ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Tumor Development ◽  
Nuclear Factor Κb ◽  
Nuclear Factor

International Variations and Trends in Renal Cell Carcinoma Incidence and Mortality

2015 ◽  
Vol 67 (3) ◽  
pp. 519-530 ◽  
Author(s):  
Ariana Znaor ◽  
Joannie Lortet-Tieulent ◽  
Mathieu Laversanne ◽  
Ahmedin Jemal ◽  
Freddie Bray
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Incidence And Mortality

scholarly journals The Ambivalent Role of miRNAs in Carcinogenesis: Involvement in Renal Cell Carcinoma and Their Clinical Applications

2021 ◽  
Vol 14 (4) ◽  
pp. 322
Author(s):  
Federica Spadaccino ◽  
Margherita Gigante ◽  
Giuseppe Stefano Netti ◽  
Maria Teresa Rocchetti ◽  
Rossana Franzin ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Transcriptional Level ◽  
Clinical Settings ◽  
Regulatory Sequences ◽  
Messenger Rnas ◽  
Physiological Processes ◽  
Target Molecules

The analysis of microRNA (miRNAs), small, non-coding endogenous RNA, plays a crucial role in oncology. These short regulatory sequences, acting on thousands of messenger RNAs (mRNAs), modulate gene expression at the transcriptional and post-transcriptional level leading to translational repression or degradation of target molecules. Although their function is required for several physiological processes, such as proliferation, apoptosis and cell differentiation, miRNAs are also responsible for development and/or progression of several cancers, since they may interact with classical tumor pathways. In this review, we highlight recent advances in deregulated miRNAs in cancer focusing on renal cell carcinoma (RCC) and provide an overview of the potential use of miRNA in their clinical settings, such as diagnostic and prognostic markers.

scholarly journals Apolipoprotein C1 stimulates the malignant process of renal cell carcinoma via the Wnt3a signaling 

2020 ◽  
Author(s):  
hao jiang ◽  
Jing-Yuan Tang ◽  
Dong Xue ◽  
Yi-Meng Chen ◽  
Ting-Chun Wu ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Nude Mice ◽  
Renal Cell ◽  
Prognostic Value ◽  
Xenograft Model ◽  
Underlying Mechanism ◽  
Clinical Samples ◽  
Incidence And Mortality

Abstract Background Renal cell carcinoma (RCC) is a clinically common tumor in the urinary system, showing an upward trend of both incidence and mortality. Apolipoprotein C1 (APOC1) has been identified as a vital regulator in tumor progression. This study aims to uncover the biological function of APOC1 in RCC process and the underlying mechanism. MethodsDifferential levels of APOC1 in RCC samples and normal tissues in a downloaded TCGA profile and clinical samples collected in our center were detected by quantitative reverse transcription PCR (qRT-PCR). The prognostic value of APOC1 in RCC was assessed by depicting Kaplan-Meier survival curves. After intervening APOC1 level by transfection of sh-APOC1 or oe-APOC1, changes in phenotypes of RCC cells were examined through CCK-8, colony formation, Transwell assay and flow cytometry. Subsequently, protein levels of EMT-related genes influenced by APOC1 were determined by Western blot. The involvement of the Wnt3a signaling in APOC1-regulated malignant process of RCC was then examined through a series of rescue experiments. Finally, a RCC xenograft model was generated in nude mice , aiming to further clarify the in vivo function of APOC1 in RCC process.ResultsAPOC1 was upregulated in RCC samples. Notably, its level was correlated to overall survival of RCC patients, displaying a certain prognostic value. APOC1 was able to stimulate proliferative, migratory and invasive abilities in RCC cells. The Wnt3a signaling was identified to be involved in APOC1-mediated RCC process. Notably, Wnt3a was able to reverse the regulatory effects of APOC1 on RCC cell phenotypes. In vivo knockdown of APOC1 in xenografted nude mice slowed down the growth of RCC.ConclusionsAPOC1 stimulates the malignant process of RCC via targeting the Wnt3a signaling.

scholarly journals Apolipoprotein C1 stimulates the malignant process of renal cell carcinoma via the Wnt3a signaling

2020 ◽  
Author(s):  
hao jiang ◽  
Jing-Yuan Tang ◽  
Dong Xue ◽  
Yi-Meng Chen ◽  
Ting-Chun Wu ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Nude Mice ◽  
Renal Cell ◽  
Prognostic Value ◽  
Xenograft Model ◽  
Underlying Mechanism ◽  
Clinical Samples ◽  
Incidence And Mortality

Abstract Background Renal cell carcinoma (RCC) is a clinically common tumor in the urinary system, showing an upward trend of both incidence and mortality. Apolipoprotein C1 (APOC1) has been identified as a vital regulator in tumor progression. This study aims to uncover the biological function of APOC1 in RCC process and the underlying mechanism. MethodsDifferential levels of APOC1 in RCC samples and normal tissues in a downloaded TCGA profile and clinical samples collected in our center were detected by quantitative reverse transcription PCR (qRT-PCR). The prognostic value of APOC1 in RCC was assessed by depicting Kaplan-Meier survival curves. After intervening APOC1 level by transfection of sh-APOC1 or oe-APOC1, changes in phenotypes of RCC cells were examined through CCK-8, colony formation, Transwell assay and flow cytometry. Subsequently, protein levels of EMT-related genes influenced by APOC1 were determined by Western blot. The involvement of the Wnt3a signaling in APOC1-regulated malignant process of RCC was then examined through a series of rescue experiments. Finally, a RCC xenograft model was generated in nude mice, aiming to further clarify the in vivo function of APOC1 in RCC process.ResultsAPOC1 was upregulated in RCC samples. Notably, its level was correlated to overall survival of RCC patients, displaying a certain prognostic value. APOC1 was able to stimulate proliferative, migratory and invasive abilities in RCC cells. The Wnt3a signaling was identified to be involved in APOC1-mediated RCC process. Notably, Wnt3a was able to reverse the regulatory effects of APOC1 on RCC cell phenotypes. In vivo knockdown of APOC1 in xenografted nude mice slowed down the growth of RCC.ConclusionsAPOC1 stimulates the malignant process of RCC via targeting the Wnt3a signaling.

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