Kidney microbiome in patients with kidney carcinoma: Role of SA and SNZ gene expression

IntroductionA kidney tumor is among the 10 most common cancers. Among kidney tumors, renal cell carcinoma (RCC) is one of the most common types with an alarming increasing incidence rate. Although the disruption of microbiota is an established factor in the progression of intestinal cancers, its role in other types of cancers has been under-studied.Material and methodsIn this study, the microbiome disruption and the involvement of SNZ (SCHNARCHZAPFEN) and SA (Stromalin) genes in the development of kidney cancer have been focused on using a combination of genetic and bioinformatic analysis. The microbiomes of kidney tumor patients were analyzed using various genetic and bioinformatic variations. Genetic and bioinformatic analyses were performed to identify operational taxonomic units (OTUs), SNZ, SA, and annotate species were determined using 41 samples from a population of kidney tumors.ResultsThe whole samples from the kidney tumor of patients were screened by PCR amplification and a total of 1317 OTUs were identified. Among them, 379 were common among the two populations, 766 were unique to the SA gene, and 172 to SNZ. SA was more abundant in Gammaproteobacteria and bacilli, while SNZ had a higher abundance in bacteroidia and actinobacteria. Correlation analysis was performed to find out the bacteria that were differentially expressed among the population samples.ConclusionsTo sum up, our study reveals that SA and SNZ are differentially expressed in the microbiome of the kidney tumor that is associated with the development of kidney tumors such as renal cell carcinoma in human populations.

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MicroRNA-384 Inhibits the Growth and Invasion of Renal Cell Carcinoma Cells by Targeting Astrocyte Elevated Gene 1

Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics ◽

10.3727/096504017x15035025554553 ◽

2018 ◽

Vol 26 (3) ◽

pp. 457-466 ◽

Cited By ~ 6

Author(s):

Haitao Song ◽

Yanwei Rao ◽

Gang Zhang ◽

Xiangbo Kong

Keyword(s):

Renal Cell Carcinoma ◽

Cell Carcinoma ◽

Renal Cell ◽

Bioinformatic Analysis ◽

Carcinoma Cells ◽

Luciferase Reporter ◽

Reporter Assay ◽

Antitumor Effects ◽

Potential Therapeutic Target

MicroRNAs (miRNAs) are emerging as pivotal regulators in the development and progression of various cancers, including renal cell carcinoma (RCC). MicroRNA-384 (miR-384) has been found to be an important cancer-related miRNA in several types of cancers. However, the role of miR-384 in RCC remains unclear. In this study, we aimed to investigate the potential function of miR-384 in regulating tumorigenesis in RCC. Here we found that miR-384 was significantly downregulated in RCC tissues and cell lines. Overexpression of miR-384 significantly inhibited the growth and invasion of RCC cells, whereas inhibition of miR-384 had the opposite effects. Bioinformatic analysis and luciferase reporter assay showed that miR-384 directly targeted the 3′-untranslated region of astrocyte elevated gene 1 (AEG-1). Further data showed that miR-384 could negatively regulate the expression of AEG-1 in RCC cells. Importantly, miR-384 expression was inversely correlated with AEG-1 expression in clinical RCC specimens. Moreover, miR-384 regulates the activation of Wnt signaling. Overexpression of AEG-1 significantly reversed the antitumor effects of miR-384. Overall, these findings suggest that miR-384 suppresses the growth and invasion of RCC cells via downregulation of AEG-1, providing a potential therapeutic target for the treatment of RCC.

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Identification of Proteins Differentially Expressed in the Conventional Renal Cell Carcinoma by Proteomic Analysis

Journal of Korean Medical Science ◽

10.3346/jkms.2005.20.3.450 ◽

2005 ◽

Vol 20 (3) ◽

pp. 450 ◽

Cited By ~ 32

Author(s):

Jeong Seok Hwa ◽

Hyo Jin Park ◽

Jae Hun Jung ◽

Sung Chul Kam ◽

Hyung Chul Park ◽

...

Keyword(s):

Renal Cell Carcinoma ◽

Cell Carcinoma ◽

Proteomic Analysis ◽

Renal Cell ◽

Differentially Expressed ◽

Conventional Renal Cell Carcinoma

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Bioinformatic analysis identifies potentially key differentially expressed genes in oncogenesis and progression of clear cell renal cell carcinoma

PeerJ ◽

10.7717/peerj.8096 ◽

2019 ◽

Vol 7 ◽

pp. e8096 ◽

Cited By ~ 2

Author(s):

Haiping Zhang ◽

Jian Zou ◽

Ying Yin ◽

Bo Zhang ◽

Yaling Hu ◽

...

Keyword(s):

Renal Cell Carcinoma ◽

Cell Carcinoma ◽

Differentially Expressed Genes ◽

Renal Cell ◽

Molecular Mechanisms ◽

Clear Cell ◽

Clinical Stage ◽

Stage I ◽

Differentially Expressed ◽

Cell Renal Cell Carcinoma

Clear cell renal cell carcinoma (ccRCC) is one of the most common and lethal types of cancer within the urinary system. Great efforts have been made to elucidate the pathogeny. However, the molecular mechanism of ccRCC is still not well understood. The aim of this study is to identify key genes in the carcinogenesis and progression of ccRCC. The mRNA microarray dataset GSE53757 was downloaded from the Gene Expression Omnibus database. The GSE53757 dataset contains tumor and matched paracancerous specimens from 72 ccRCC patients with clinical stage I to IV. The linear model of microarray data (limma) package in R language was used to identify differentially expressed genes (DEGs). The protein–protein interaction (PPI) network of the DEGs was constructed using the search tool for the retrieval of interacting genes (STRING). Subsequently, we visualized molecular interaction networks by Cytoscape software and analyzed modules with MCODE. A total of 1,284, 1,416, 1,610 and 1,185 up-regulated genes, and 932, 1,236, 1,006 and 929 down-regulated genes were identified from clinical stage I to IV ccRCC patients, respectively. The overlapping DEGs among the four clinical stages contain 870 up-regulated and 645 down-regulated genes. The enrichment analysis of DEGs in the top module was carried out with DAVID. The results showed the DEGs of the top module were mainly enriched in microtubule-based movement, mitotic cytokinesis and mitotic chromosome condensation. Eleven up-regulated genes and one down-regulated gene were identified as hub genes. Survival analysis showed the high expression of CENPE, KIF20A, KIF4A, MELK, NCAPG, NDC80, NUF2, TOP2A, TPX2 and UBE2C, and low expression of ACADM gene could be involved in the carcinogenesis, invasion or recurrence of ccRCC. Literature retrieval results showed the hub gene NDC80, CENPE and ACADM might be novel targets for the diagnosis, clinical treatment and prognosis of ccRCC. In conclusion, the findings of present study may help us understand the molecular mechanisms underlying the carcinogenesis and progression of ccRCC, and provide potential diagnostic, therapeutic and prognostic biomarkers.

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Peer Review #1 of "Integrated analysis of differentially expressed profiles and construction of a competing endogenous long non-coding RNA network in renal cell carcinoma (v0.1)"

10.7287/peerj.5124v0.1/reviews/1 ◽

2018 ◽

Keyword(s):

Renal Cell Carcinoma ◽

Cell Carcinoma ◽

Peer Review ◽

Renal Cell ◽

Differentially Expressed ◽

Integrated Analysis ◽

Non Coding Rna ◽

Long Non Coding Rna

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Identification and Classification of Differentially Expressed Genes in Renal Cell Carcinoma by Expression Profiling on a Global Human 31,500-Element cDNA Array

Genome Research ◽

10.1101/gr.184501 ◽

2001 ◽

Vol 11 (11) ◽

pp. 1861-1870 ◽

Cited By ~ 125

Author(s):

Judith M. Boer ◽

Wolfgang K. Huber ◽

Holger Sültmann ◽

Friederike Wilmer ◽

Anja von Heydebreck ◽

...

Keyword(s):

Renal Cell Carcinoma ◽

Cell Carcinoma ◽

Differentially Expressed Genes ◽

Expression Profiling ◽

Renal Cell ◽

Cdna Array ◽

Differentially Expressed

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Birt-Hogg-Dubé Syndrome: Clinicopathologic Findings and Genetic Alterations

Archives of Pathology & Laboratory Medicine ◽

10.5858/2006-130-1865-bscfag ◽

2006 ◽

Vol 130 (12) ◽

pp. 1865-1870 ◽

Cited By ~ 7

Author(s):

Brian P. Adley ◽

Norm D. Smith ◽

Ritu Nayar ◽

Ximing J. Yang

Keyword(s):

Renal Cell Carcinoma ◽

Cell Carcinoma ◽

Renal Cell ◽

English Literature ◽

Clinical Manifestations ◽

Genetic Alterations ◽

Limited Information ◽

Kidney Tumors ◽

Pulmonary Cysts ◽

Bhd Syndrome

Abstract Context.—Birt-Hogg-Dubé (BHD) syndrome is a rare clinicopathologic condition transmitted in an autosomal dominant fashion. This complex entity is characterized by cutaneous fibrofolliculomas, kidney tumors, pulmonary cysts, and spontaneous pneumothorax. Recently, the gene possibly responsible for the clinical manifestations of BHD syndrome has been cloned and characterized. The few reviews of BHD syndrome found in the English literature mostly focus on the skin lesions or genetics, with limited information on other pathologic changes, particularly the kidney lesions. Objective.—To review the literature on this subject with a special emphasis on BHD syndrome-associated renal pathology as well as recent advances in molecular genetic discovery of the BHD syndrome. Data Sources.—We used all data available after performing a literature search using MEDLINE and searching under the headings “Birt-Hogg-Dubé,” “hybrid oncocytic tumors,” and “folliculin.” Conclusions.—The presence of BHD syndrome should be investigated in any patient with multiple bilateral kidney tumors, especially if the predominant histologic type is chromophobe renal cell carcinoma or the so-called hybrid oncocytic tumor. The genetic alteration for BHD syndrome has been mapped to chromosome 17p12q11, and the gene in this region has been cloned and believed to be responsible for the BHD syndrome. The function of the BHD product, called folliculin, is still unknown, although it is speculated to be a tumor suppressor gene. Numerous mutations have been described in the BHD gene. Studies are ongoing to determine the relationship between the BHD gene and development of sporadic renal cell carcinoma and other lesions.

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Renal oncocytoma: Personal experience

Urologia Journal ◽

10.1177/039156039205901s52 ◽

1992 ◽

Vol 59 (1_suppl) ◽

pp. 156-159

Author(s):

S. Invernizzi ◽

D. Pozza ◽

G. Longo ◽

S. Cappoli ◽

G. Locatelli ◽

...

Keyword(s):

Renal Cell Carcinoma ◽

Cell Carcinoma ◽

Renal Cell ◽

Personal Experience ◽

Renal Oncocytoma ◽

Kidney Tumors ◽

Immunohistochemical Reaction

The Authors report their experience on kidney oncocytomas. They found 6 cases of kidney oncocytoma in 140 cases of kidney tumors. In all cases histological slides of neoplastic masses were made with traditional stains, PAS and PAS diastase and with immunohistochemical reaction for keratins (BDK) and vimentin (DAKO clone V9). They describe one of the six cases in which the diagnosis of oncocitary G3 type carcinoma was made, and another of oncocytomatosis with borderline aspects versus oncocytomal renal cell carcinoma.

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The level of FSHR expression in the primary kidney tumors to predict the response to subsequent antiangiogenic therapy with sunitinib.

Journal of Clinical Oncology ◽

10.1200/jco.2012.30.15_suppl.e21138 ◽

2012 ◽

Vol 30 (15_suppl) ◽

pp. e21138-e21138

Author(s):

Muhammad Ahsan Siraj ◽

Christophe Pichon ◽

Aurelian Radu ◽

Nicolae Ghinea

Keyword(s):

Renal Cell Carcinoma ◽

Cell Carcinoma ◽

Sensitivity And Specificity ◽

Renal Cell ◽

Kinase Inhibitor ◽

Antiangiogenic Therapy ◽

Total Density ◽

Kidney Tumors ◽

Cell Renal Cell Carcinoma ◽

Primary Tumors

e21138 Background: Sunitinib is an antiangiogenic receptor tyrosine kinase inhibitor used to treat advanced metastatic renal cell carcinoma and other types of cancer. Sunitinib is effective in only approx. 70% of clear cell renal cell carcinoma (CCRCC) patients, has significant adverse side effects, and no method is available to predict which patients will not respond. Our purpose was to explore the possibility of introducing an effective prediction method based on a marker of the tumor vasculature, the Follicle Stimulating Hormone Receptor (FSHR). Methods: Using immunohistochemistry on paraffin sections with anti-FSHR monoclonal antibodies we studied by photonic and fluorescence microscopy the expression of FSHR in 50 patients diagnosed with advanced metastatic CCRCC. All patients were subjected to surgery for removal of the primary tumor and were subsequently treated with sunitinib orally for ≥ 3 months with a dose of 50 mg/day for 4 weeks followed by 2 weeks off. After therapy the patients were categorized as “responsive”, “stable”, or “non-responsive” based on the RECIST guidelines. The blood vessel density and the percentage of FSHR-positive vessels were determined by immunofluorescence on sections from the primary tumors removed by surgery, prior to the sunitinib treatment. Von Willebrand factor (vWF) was used as specific endothelial marker. Results: There were no significant differences in the total density of vessels (detected with anti-vWF antibody) among the responsive, stable and non-responsive patients. The percentage of FSHR-stained vessels was on average five fold higher for the patients that responded to the treatment in comparison with the stable group and almost eight fold higher than in the non-responsive group. The percentage allowed the detection of responders with 87-100% sensitivity and specificity. Conclusions: The data suggest that FSHR expression levels in the blood vessels of CCRCC primary tumors can be used to predict, with high sensitivity and specificity, the patients that will respond to sunitinib therapy.

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