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The mechanism of elevated S100A6 (Calcyclin) Enhances Tumorigenesis in clear cell renal cell carcinoma

ABSTRACT: Among all types of urological cancers, the clear cell renal cell carcinoma is the second leading cause of death in adults. This is mainly due to lack of promising prognosis or predictors, and effective target therapy. S100A6 (calcyclin), a member of S100 family of proteins, is reported to be elevated in many types of cancers. In the present study, we analyzed the expression of S100A6 in mRNA, in proteins and tissues. The mechanism of enhancing tumorigenesis was studied to understand the role of S100A6 in clear cell renal cell carcinoma tumorigenesis. Microarray and bioinformatic analyses were performed in the stable transfection of overexpression and knockdown of S100A6, comparing with each empty vector control in order to find the different expression genes and explore the mechanism. The microarray analysis of clear cell renal cell carcinoma 786-O cell line treated with overexpression and knockdown S100A6.

ORGANISM(S): Homo sapiens

PROVIDER: GSE52708 | GEO | 2013/11/25

SECONDARY ACCESSION(S): PRJNA229870

REPOSITORIES: GEO

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The mechanism of elevated S100A6 (Calcyclin) Enhances Tumorigenesis in clear cell renal cell carcinoma

Project description:Among all types of urological cancers, the clear cell renal cell carcinoma is the second leading cause of death in adults. This is mainly due to lack of promising prognosis or predictors, and effective target therapy. S100A6 (calcyclin), a member of S100 family of proteins, is reported to be elevated in many types of cancers. In the present study, we analyzed the expression of S100A6 in mRNA, in proteins and tissues. The mechanism of enhancing tumorigenesis was studied to understand the role of S100A6 in clear cell renal cell carcinoma tumorigenesis. Microarray and bioinformatic analyses were performed in the stable transfection of overexpression and knockdown of S100A6, comparing with each empty vector control in order to find the different expression genes and explore the mechanism. The microarray analysis of clear cell renal cell carcinoma 786-O cell line treated with overexpression and knockdown S100A6. Four samples: overexpression S100A6 sample and vector control sample, knockdown S100A6 and vector control sample, each sample had three replicates.

2013-11-25 | E-GEOD-52708 | biostudies-arrayexpress

Homo sapiens

Project description:The mechanism of elevated S100A6 (Calcyclin) Enhances Tumorigenesis in clear cell renal cell carcinoma

| PRJNA229870 | ENA

HAVCR/KIM-1 activates the IL-6/STAT-3 Pathway in ccRCC and Determines Tumor Progression and Patient Outcome

Project description:Renal cell carcinoma (RCC), the third most prevalent urological cancer, claims more than 100,000 lives/year worldwide. The clear cell (ccRCC) is the most common and aggressive subtype of renal cancer. Commonly asymptomatic, more than 30% of ccRCCs are diagnosed when they are already metastatic resulting in a 95% mortality rate and one-third of organ-confined cancers treated by nephrectomy develop metastasis during the follow-up. Diagnosis and monitoring requires expensive and frequent imaging examinations; thereby, finding of diagnostic and prognostic biomarkers to screen, diagnose and monitor renal cancers are clearly needed. Hepatitis A virus receptor/kidney injury molecule 1 (HAVCR1/KIM-1) gene has been claimed to be a susceptibility gene for ccRCC and HAVCR1/KIM-1 ectodomain shedding a predictive biomarker of tumor progression.

2020-09-27 | E-MTAB-2071 | biostudies-arrayexpress

Expression data from human clear-cell renal cell carcinoma cell line 769-P after overexpression of FOXK2

Project description:Clear-cell renal cell carcinoma (ccRCC) is one of the most common urological malignant neoplasms. In addition, ccRCC is a highly aggressive cancer with a concomitant poor prognosis. Forkhead box K2 (FOXK2) has been reported to involve in many molecular mechanisms.However, little is known about the role FOXK2 plays in clear-cell renal cell carcinoma. Our previous study showed that FOXK2 mRNA and protein expression were decreased in human ccRCC tissues and suppressed the proliferation of ccRCC cells both in vitro and in vivo. We used microarrays (Affymetrix HTA2.0 Array) to detail the differentially expressed genes after overexpression of FOXK2, and aim to find potential one or more target gene/genes of FOXK2

2016-12-23 | GSE92777 | GEO

SIRT3 Deacetylates TFAM to Promote Mitochondrial Biogenesis

Project description:SIRT3 is a NAD+-dependent mitochondrial protein deacetylase participating in the regulation of central metabolism and mitochondrial proteostasis. SIRT3 is downregulated in clear cell renal cell carcinoma (ccRCC), a main type of renal cancers, but the function of SIRT3 in tumorigenesis and development of ccRCC remains unknown. In this study, we established a SIRT3 overexpressed cell line to explore the changes of proteomics and metabolomics regulated by SIRT3 expression. Both the results of quantitative proteomics, metabolomics and acetylome showed overexpression of SIRT3 increased mitochondrial biogenesis and reversed the mitochondrial dysfunctions in ccRCC. We found SIRT3 could increase the activity of TFAM through modulation of TFAM transcription, degradation and acetylation level. The acetylation of TFAM K154 decreased while TFAM protein expression increased after SIRT3 overexpression. Further study revealed that SIRT3 could bind with TFAM, and decrease the acetylation of TFAM, promoting TFAM activity in mitochondrial biogenesis. Overall, our results present a new mechanism of SIRT3 in regulating mitochondrial functions, and the downregulation of SIRT3 in ccRCC lowers the activity of TFAM, subsequently inhibits the transcription of mitochondrial genes and mitochondrial biogenesis.

2018-08-14 | PXD009110 | Pride

MicroRNA expression data from human renal cell cancer subtypes

Project description:MicroRNAs play a vital role in the process of tumorigenesis. To identify and characterize miRNA Expression in renal cell cancer, we performed microarray based screening of miRNA expression profiles in clear cell, papillary type 1 and papillary type 2 renal cell cancer. We selected cases of confirmed clear cell, papillary type 1 and papillary type 2 renal cell carcinoma and generated pairs of tumor and corresponding normal tissue by manual microdissection.

2012-10-03 | E-GEOD-41282 | biostudies-arrayexpress

The deubiquitylating enzyme USP35 restricts regulated cell death to promote survival of renal clear cell carcinoma

Project description:The ubiquitin proteasome system governs a wide spectrum of cellular events and offers therapeutic opportunities for pharmacological intervention in cancer treatment. Renal clear cell carcinoma represents the predominant histological subtype and accounts for the majority of cancer death related to kidney malignancies. Through a systematic survey in the association of human ubiquitin-specific proteases with patient prognosis of renal clear cell carcinoma and subsequent phenotypic validation, we uncovered the tumor-promoting role of USP35. Biochemical characterizations confirmed the stabilizing effects of USP35 towards multiple members of the IAP family in an enzymatic activity-dependent manner. USP35 silencing led to reduced expression levels of IAP proteins, which were accompanied with increased cellular apoptosis. Further transcriptomic analysis revealed that USP35 knockdown altered expression levels of NRF2 downstream transcripts, which were conferred by compromised NRF2 abundance. USP35 functions to maintain NRF2 levels by catalyzing its deubiquitylation and thus antagonizing degradation. NRF2 reduction imposed by USP35 silencing rendered renal clear cell carcinoma cells increased sensitivity to ferroptosis induction. Finally, induced USP35 knockdown markedly attenuated xenograft formation of renal clear cell carcinoma in nude mice. Hence, our findings identify a number of USP35 substrates and reveal the protecting role of USP35 against both apoptosis and ferroptosis in renal clear cell carcinoma.

2023-06-17 | GSE216154 | GEO

Remodeling of major genomic fabrics and their interplay in metastatic clear cell renal carcinoma

Project description:Clear cell renal carcinoma (CCRC) accounts for >80% of all kidney cancers but what triggers the tumorigenesis in the kidney and metastases in the bones are still under debate. Our hypothesis is that remodeling of the genomic fabrics of certain functional pathways and their interplay beyond critical limits are key causes of CCRC. We profiled the transcriptomes of metastatic chest wall and of two primary cancerous sites of the renal medulla and compared them with that of non-cancerous kidney resection margins. Samples were collected from a 74 years old male with metastatic carcinoma, consistent with renal cell carcinoma, clear cell type, Fuhrman grade 3, who undergone total right kidney nephrectomy and resection of a chest wall mass. Transcriptomic analysis pointed the tumor region in the right kidney that led to the chest wall metastases. The tumor proved heterogeneous not only in the expression level but also in the expression control, coordination and interplay of pathways responsible for cellular processes and genetic and environmental information processing. The differently regulated pathways in the two sides of the tumor: CCRC, and HIF-1, Vegfa and mTor signaling indicate activation of distinct mechanisms. Four-conditions (CTR = control - non-cancerous kidney resection margins, PTA = primary tumor side A, PTB = primary tumor side B, MET = chest wall metastasis. Four biological replicates of each condition.

2015-08-24 | E-GEOD-72304 | biostudies-arrayexpress

Project description:RNA-seq of clear renal cell carcinoma after PBRM1 knockdown

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Expression data from patients with different stages of clear cell renal cell carcinoma

Project description:Clear cell renal cell carcinoma is the most common type of renal cancers, which forms tumors strongly supplied with blood vessels, here we wanted to check the exprresion of genes on different stages of tumor progression, and find which of them changes significantly with increased grade.

2016-11-05 | GSE89563 | GEO

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