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Gene expression analysis of kidney primary tubular epithelial cells (PTECs), SETD2-KD PTECs, PBRM1-KD PTECs and ccRCC derived cell lines

ABSTRACT: Transcriptional profiling of human WT-PTECs, SETD2-KD PTECs, PBRM1-KD PTECs, and 10 different ccRCC derived cell lines. ccRCC derived cell lines showed distict expression signatures as compared to PTECs, some of them also present in SETD2-KD PTECs, and/or PBRM1-KD PTECs.

ORGANISM(S): Homo sapiens

PROVIDER: GSE89214 | GEO | 2017/11/01

SECONDARY ACCESSION(S): PRJNA350686

REPOSITORIES: GEO

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Gene expression analysis of untreated and NT-shRNA transduced kidney proximal tubular epithelial cells (PTECs) at day 6 and day 16 after transduction, as well as SETD2-shRNA transduced PTECs at day 25 after transduction.

Project description:Primary kidney PTECs gradually became senescesince day 16, but SETD2 depletion prevented PTECs from senescence and maintained their proliferation beyond their limited dividing capacity. Transcriptional profiling of human PTECs, with comparing of non-senescent PTECs (PTECs-day 6), senescent PTECs (PTECs-day16), and SETD2 depleted PTECs at day 25 (SETD2 KD-PTECs-day 25). Three PTECs of different origins were transduced with shRNA constructs against SETD2 (sh1 or sh2), or with a non-targeting sequence. Untreated and NT-shRNA transduced samples were harvest at day 6 and day 16 respectively, SETD2-KD shRNA transduced PTECs were harvest at day 25.

2016-01-09 | E-GEOD-72792 | biostudies-arrayexpress

Proteomics analysis on SETD2 loss induced ccRCC formation

Project description:Patients with polycystic kidney disease (PKD) encounter a high risk of clear cell renal cell carcinoma (ccRCC), a malignant tumor with dysregulated lipid metabolism. SET domain–containing 2 (SETD2) has been identified as an important tumor suppressor gene in ccRCC. However, the role of SETD2 in tumorigenesis during the transition from PKD to ccRCC remains largely unexplored. Herein, we performed metabolomics, lipidomics, transcriptomics and proteomics with SETD2 loss induced PKD-ccRCC transition mouse model. To characterize biological responses triggered by SETD2 deletion during PKD-ccRCC transition at the protein level, we conducted global proteomics studies.

2023-10-31 | PXD038966 | Pride

Project description:Primary kidney PTECs gradually became senescent after a few passages, but SETD2 depletion prevented PTECs from senescence and maintained their proliferation beyond their limited dividing capacity. Transcriptional profiling of human PTECs, with comparing of SETD2 wild-type non-senescent PTECs at day 6 (WT-PTECs-day 6), SETD2 wild-type senescent PTECs at day 16 (WT-PTECs-day16), and SETD2 knockdown PTECs at day 25 (KD-PTECs-day 25).

2016-01-09 | GSE72792 | GEO

The effects of PBRM1 loss on the ccRCC transcriptome

Project description:Subunits of SWI/SNF chromatin remodeling complexes are frequently mutated in human malignancies. The PBAF complex is composed of multiple subunits, including the tumor suppressor protein PBRM1 (BAF180), as well as ARID2 (BAF200), that are unique to this SWI/SNF complex. PBRM1 is mutated in various cancers, with a high mutation frequency in clear cell renal cell carcinoma (ccRCC). In this study, we integrate RNA-seq, histone modification ChIP-seq, and ATAC-seq data to show that loss of PBRM1 results in de novo gains in H3K4me3 peaks throughout the epigenome including activation of a retinoic acid biosynthesis and signaling gene signature. We show that one such target gene, ALDH1A1, which regulates a key step in retinoic acid biosynthesis, is consistently upregulated with PBRM1 loss in ccRCC cell lines and primary tumors, as well as non-transformed cells. We further find that ALDH1A1 increases the tumorigenic potential of ccRCC cells. Using biochemical methods, we show that ARID2 remains bound to other PBAF subunits after loss of PBRM1 and is essential for increased ALDH1A1 after loss of PBRM1, whereas other core SWI/SNF components are dispensable, including the ATPase subunit BRG1. In total, this study uses global epigenomic approaches to uncover novel mechanisms of PBRM1 tumor suppression in ccRCC.

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Homo sapiens

Project description:Gene expression analysis of kidney primary tubular epithelial cells (PTECs), SETD2-KD PTECs, PBRM1-KD PTECs and ccRCC derived cell lines

| PRJNA350686 | ENA

RNA-sequencing of renal cells from Setd2-wildtype PKD and Setd2-knlckout ccRCC mice.

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Project description:SETD2, a H3K36 trimethyltransferase, is frequently mutated in human cancers with the highest prevalence (13%) in clear cell renal cell carcinoma (ccRCC). Genomic profiling of primary ccRCC tumors reveals a positive correlation between SETD2 mutations and metastasis. However, whether and how SETD2-loss promotes metastasis remains unclear. Here, we detected SETD2 mutations in 24 of 51 (47%) metastatic ccRCC tumors. Using SETD2-mutant metastatic ccRCC patient-derived cell line and xenograft models, we showed that H3K36me3 restoration greatly reduced distant metastases of ccRCC in mice. An integrated ATAC-seq, ChIP-seq, and transcriptome analysis concluded a tumor suppressor model in which loss of SETD2-mediated H3K36me3 activates enhancers to drive oncogenic transcription through dysregulating histone chaperone recruitment, enhancing histone exchange, and expanding chromatin accessibility. Furthermore, we uncovered mechanism-based therapeutic strategies for SETD2-deficient cancer through inhibition of histone chaperones. Overall, SETD2-loss creates a permissive epigenetic landscape for cooperating oncogenic drivers to amplify transcriptional output, providing unique therapeutic opportunities.

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Gene expression analysis of ccRCC cell line upon SETD2 rescue [RNAseq_JHRCC12]

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Genome binding/occupancy profiling of ccRCC cell line upon SETD2 rescue [ChIPseq_JHRCC12]

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DNA Copy-Number Alterations in clear-cell Renal Cell Carcinoma (ccRCC) Tumors and Tumorgrafts for samples deficient in BAP1 or PBRM1

Project description:Renal cell carcinoma (RCC) exhibits some unusual features and genes commonly mutated in cancer are rarely mutated in clear-cell RCC (ccRCC), the most common type. The most prevalent genetic alteration in ccRCC is the inactivation of the tumor suppressor gene VHL. Using whole-genome and exome sequencing we discovered BAP1 as a novel tumor suppressor in ccRCC that shows little overlap with mutations in PBRM1, another recent tumor suppressor. Whereas VHL was mutated in 81% of the patients (142/176), PBRM1 was lost in 58% and BAP1 in 15% of the patients analyzed. All these tumor suppressor genes are located in chromosome 3p, which is partially or completely lost in most ccRCC patients. However, BAP1 but not PBRM1 loss was associated with higher Fuhrman grade and, therefore, poorer outcome. Xenograft tumors (tumorgrafts) implanted orthotopically in mice retained >92% of mutations and exhibited similar DNA copy number alterations to corresponding primary tumors. Thus, after inactivation of VHL, the acquisition of a mutation in BAP1 or PBRM1 defines a different program that might alter the fate of the patient. Our results establish the foundation for an integrated pathological and molecular genetic classification of about 70% of ccRCC patients, paving the way for subtype-specific treatments exploiting genetic vulnerabilities. The genomic DNA of clear-cell renal cell carcinoma (ccRCC) primary tumors, tumors growing in immunodeficient mice (tumorgrafts), and normal samples were labeled and hybridized to Affymetrix SNP arrays 6.0.

2012-06-09 | E-GEOD-25540 | biostudies-arrayexpress

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