Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Proteomic Analysis in MAFF-knockdown 786-O and Caki-1 Cells

ABSTRACT: This project comprises a comparative proteomic analysis of MAFF-knockdown and control 786-O and Caki-1 human renal cancer cell lines. The data aims to identify protein targets and signaling pathways regulated by MAFF in ccRCC, providing critical insights into the mechanism by which MAFF influences tumor biology and progression.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Permanent Cell Line Cell, Cell Culture

DISEASE(S): Renal Clear Cell Carcinoma,Kidney Cancer

SUBMITTER: Vic Un

LAB HEAD: Waikeong Un

PROVIDER: PXD068979 | Pride | 2026-07-09

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	checksum.txt	Txt
	db.peptides.csv.zip	Csv
	db.proteins.csv.zip	Csv
	raw_files_all.zip	Other

Items per page:

1 - 4 of 4

Similar Datasets

Proteomic Analysis in Renca Cells with Smarcd1 Overexpression or Knockdown Compared to Controls

Project description:In this study, we performed a proteomic analysis on Renca cells to investigate the impact of SMARCD1 overexpression and knockdown. This dataset provides a comprehensive view of protein-level changes and helps to validate the role of SMARCD1 in ccRCC.

2026-07-09 | PXD068898 | Pride

Expression data from 786-O renal cell cancer cells treated with pentamidine

Project description:While early stages of clear cell renal cell carcinoma (ccRCC) are curable, survival outcome for metastatic ccRCC remains poor. The purpose of the current study was to apply a new individualized bioinformatics analysis (IBA) strategy to these transcriptome data in conjunction with Gene Set Enrichment Analysis of the Connectivity Map (C-MAP) database to identify and reposition FDA-approved drugs for anti-cancer therapy. We demonstrated that one of the drugs predicted to revert the RCC gene signature towards normal kidney, pentamidine, is effective against RCC cells in culture and in a RCC xenograft model. Most importantly, pentamidine slows tumor growth in the 786-O human ccRCC xenograft mouse model. To determine which genes are regulated by pentamidine in a human RCC cell line, 786-O, we treated these cells with pentamidine and performed transcriptional profiling analysis. We used microarrays to determine the set of genes regulated by pentamidine in 786-O renal cell cancer cells. Total RNA was isolated from 786-O cells treated with 25 Î¼M pentamidine or vehicle control (DMSO) for 6 hours and hybridized to Affymetrix microarrays.

2014-08-05 | E-GEOD-54709 | biostudies-arrayexpress

SMARCD1 Affinity Purification-mass Spectrometry (AP-MS) in HEK-293 Cells

Project description:This study reports the identification of the FLAG-tagged SMARCD1 protein interactome in HEK-293 cells using Affinity Purification-Mass Spectrometry (AP-MS). The data provides a comprehensive list of proteins that physically associate with SMARCD1, thereby contributing to the understanding of its molecular functions and regulatory complexes.

2026-07-09 | PXD068854 | Pride

Genome-wide identification of transcriptional targets for H4K12 lactylation in ccRCC cells

Project description:To investigate the genome-wide transcription targets of H4K12 lactylation in ccRCC cells, cleavage under targets and tagmentation (CUT&Tag) was performed in 786-O and Caki-1 cells using antibody against H4K12 lactylation. Following CUT&Tag, DNAs were amplified using non-biased conditions, labeled, and sequenced with Illumina NovaSeq 150PE.

2026-01-23 | GSE315326 | GEO

Expression data from 786-O renal cell cancer cells treated with pentamidine

2014-08-05 | GSE54709 | GEO

Next Generation Sequencing of 786-O-Ctrl and786-O-VHL Transcriptomes

Project description:Inactivation of the E3 ubiquitin ligase protein von Hippel-Lindau (VHL) is critical to clear cell renal cell carcinomas (ccRCC) and VHL syndrome. VHL loss leads to stabilization of hypoxia-inducible factor α (HIFα) and other substrate proteins, which may drive various tumor-promoting pathways. This process is likely reversible, because even in the highly aggressive human VHL-deficient ccRCC cell line 786-O, restoring VHL expression almost completely abolishes orthotopic tumor formation in immuno-deficient mice. This result highlights the potential of treating ccRCC by re-expressing VHL with gene therapy. However, there is inadequate understanding of the consequence of VHL restoration at the molecular level. Here, we reinstalled VHL expression in 786-O and performed transcriptome, proteome and ubiquitome profiling to assess the molecular impact.

2021-10-18 | GSE186013 | GEO

Genome wide expression change by 786-O cells treated with MST1/2 inhibitor XMU-MP-1

Project description:We aim to the investigate the role of MST1/2 inhibitor XMU-MP-1 in kindy renal clear cell carcinoma (ccRCC) progression. 786-O cells were used as the model.

2022-02-28 | GSE197468 | GEO

786-O and 786-VHL in EMCV study

2010-06-10 | GSE22256 | GEO

786-O and 786-VHL in EMCV study

Project description:786-0 is a cell line derived from a clear cell renal carcinoma. Previous studies have shown that the 786-O cell line harbors an inactivating mutation in the von-Hippel Lindau (VHL) gene. Mutations in the VHL gene occur in the majority of sporadic clear cell renal cell. To determine how inactivation of the VHL affects cellular functions, we created a derivative of 786-0, which we call 786-VHL in which a functional allele of VHL has been introduced back into the 786-O cell line. The renal cell carcinoma cell line 786-0, which harbors a mutated allele of VHL, was compared to a cell line derived from 786-0, termed 786-VHL, that contains a functional allele of VHL. Genes whose expression characteristics were dependent on functional VHL were identified.

2010-06-23 | E-GEOD-22256 | biostudies-arrayexpress

Gene expression changes in 786-O cells in response to 5DC treatment.

Project description:Inactivation of the von Hippel-Lindau tumor suppressor gene, VHL, is an archetypical tumor-initiating event in clear cell renal carcinoma (ccRCC) that leads to the activation of hypoxia-inducible transcription factors (HIFs). However, VHL mutation status in ccRCC is not correlated with clinical outcome. Here we show that during ccRCC progression, cancer cells exploit diverse epigenetic alterations to empower a branch of the VHL-HIF pathway for metastasis, and the strength of this activation is associated with poor clinical outcome. By analyzing metastatic subpopulations of VHL-deficient ccRCC cells, we discovered an epigenetically altered VHL-HIF response that is specific to metastatic ccRCC. Focusing on the two most prominent pro-metastatic VHL-HIF target genes, we show that loss of polycomb repressive complex 2 (PRC2)-dependent histone H3 Lys27 trimethylation (H3K27me3) activates HIF-driven chemokine (C-X-C motif) receptor 4 (CXCR4) expression in support of chemotactic cell invasion, whereas loss of DNA methylation enables HIF-driven cytohesin 1 interacting protein (CYTIP) expression to protect cancer cells from death cytokine signals. Thus, metastasis in ccRCC is based on an epigenetically expanded output of the tumor-initiating pathway. Gene expression data from 786-O cells after 3-day treatment with 100uM 5’-aza-deoxycytidine (5DC) or vehicle (DMSO).

2012-12-05 | E-GEOD-32298 | biostudies-arrayexpress