{"database":"Pride","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Txt":["ftp://ftp.pride.ebi.ac.uk/pride/data/archive/2026/06/PXD069813/checksum.txt"],"Raw":["ftp://ftp.pride.ebi.ac.uk/pride/data/archive/2026/06/PXD069813/G2-CD70-KO-3.raw","ftp://ftp.pride.ebi.ac.uk/pride/data/archive/2026/06/PXD069813/G1-Ctrl-2.raw","ftp://ftp.pride.ebi.ac.uk/pride/data/archive/2026/06/PXD069813/G3-CD70-mAb-4.raw","ftp://ftp.pride.ebi.ac.uk/pride/data/archive/2026/06/PXD069813/G2-CD70-KO-5.raw","ftp://ftp.pride.ebi.ac.uk/pride/data/archive/2026/06/PXD069813/G1-Ctrl-4.raw","ftp://ftp.pride.ebi.ac.uk/pride/data/archive/2026/06/PXD069813/G2-CD70-KO-1.raw","ftp://ftp.pride.ebi.ac.uk/pride/data/archive/2026/06/PXD069813/G3-CD70-mAb-1.raw","ftp://ftp.pride.ebi.ac.uk/pride/data/archive/2026/06/PXD069813/G1-Ctrl-3.raw","ftp://ftp.pride.ebi.ac.uk/pride/data/archive/2026/06/PXD069813/G3-CD70-mAb-5.raw","ftp://ftp.pride.ebi.ac.uk/pride/data/archive/2026/06/PXD069813/G2-CD70-KO-4.raw","ftp://ftp.pride.ebi.ac.uk/pride/data/archive/2026/06/PXD069813/G1-Ctrl-1.raw","ftp://ftp.pride.ebi.ac.uk/pride/data/archive/2026/06/PXD069813/G3-CD70-mAb-3.raw","ftp://ftp.pride.ebi.ac.uk/pride/data/archive/2026/06/PXD069813/G2-CD70-KO-2.raw","ftp://ftp.pride.ebi.ac.uk/pride/data/archive/2026/06/PXD069813/G1-Ctrl-5.raw","ftp://ftp.pride.ebi.ac.uk/pride/data/archive/2026/06/PXD069813/G3-CD70-mAb-2.raw"],"Fasta":["ftp://ftp.pride.ebi.ac.uk/pride/data/archive/2026/06/PXD069813/uniprotkb_Human_AND_model_organism_9606_2023_12_17.fasta"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"labhead_mail":["Jie.Ni22@student.xjtlu.edu.cn"],"submitter":["Jie Ni"],"technology_type":["Mass Spectrometry","Bottom-up proteomics"],"disease":["Renal Clear Cell Carcinoma"],"software":[""],"submitter_keywords":["Ras/erk pathway","Cd70","Proteomics","Nf1","Metastasis","Combination therapy","Ccrcc","Emt"],"full_dataset_link":["https://www.ebi.ac.uk/pride/archive/projects/PXD069813"],"tissue":["Permanent Cell Line Cell","Cell Culture"],"sample_protocol":["Cells from three groups were cultured in T175 flasks (~1×106 cells per flask). Upon reaching the appropriate confluence, cells from five independent biological replicates were harvested and subjected to lysis with a urea-based buffer composed of 8 M urea, 1% (v/v) protease inhibitor cocktail and 2 mM EDTA at room temperature. The lysates underwent three cycles of sonication. The resulting lysates were centrifugated at 12,000×g for 20 min at 4 ℃, and the supernatants were carefully transferred to fresh tubes. Protein concentrations were determined using the BCA Protein Assay Kit. Prior to digestion, proteins were first reduced with 5 mM dithiothreitol (DTT) at 56℃ for 30 min and subsequently alkylated with 10 mM iodoacetamide at RT for 30 min in the dark. Urea concentration was then diluted to 1 M with 50 mM ammonium bicarbonate (ABC) buffer, followed by overnight trypsin digestion (1:75 w/w enzyme-to-substrate ratio) at 37℃. Post-digestion, samples were centrifuged at 2,000×g for 10 min, and the supernatant was desalted using a MonoSpin C18 Purification column prior to lyophilization.  Mass spectrometry-based proteomics analysis was performed using a Thermo Vanquish Neo UHPLC system coupled to a Q-Exactive Plus Orbitrap mass spectrometer (Thermo Fisher Scientific). Peptide separation was performed on a DNV PepMap Neo C18 column (2 µm particle size, 75 µm × 150 mm) using a 165-min gradient elution at a constant flow rate of 300 nL/min."],"repository":["Pride"],"quantification_method":[""],"modification":[""],"data_protocol":["Proteome Discoverer Software (Version 2.5) was used for label-free quantitation (LFQ) analysis. Only proteins identified with ≥2 unique peptide were included in subsequent analysis. The false discovery rate (FDR) cut-off value was set to 0.05 across all analyses. For comprehensive data validation, raw LFQ intensity data were further processed using R software (version 4.3.2) with the following bioinformatics packages: limma (version 3.52.2) for differential expression analysis, and clusterProfiler (version 4.4.4) for Gene Ontology (GO) enrichment analysis [17]. To be considered significant, differentially expressed proteins (DEPs) were required to meet the following criteria: adjusted p-value of less than 0.05 and absolute fold change (|FC|) of more than 2 when comparing either CD70-KO or CD70 mAb-treated samples with Ctrl samples. The overlap of up-regulated DEPs across both datasets was generated by Venn diagram. Further functional enrichment analyses, including GO and Kyoto Encyclopedia of Genes and Genomes (KEGG), were performed using R to investigate the biological pathways associated with dysregulated proteins."],"omics_type":["Proteomics"],"labhead":["Jie Ni"],"instrument_platform":[""],"labhead_affiliation":["Academy of Pharmacy, Xi’an Jiaotong-Liverpool University, Suzhou, Jiangsu 215123, China"],"submission_type":["PARTIAL"],"species":["Homo Sapiens (human)"],"submitter_mail":["jie.ni22@student.xjtlu.edu.cn"],"publication":["41882700 Ni J, Gao A, Chen Y, He C, Wang X, Savelyeva N, Dong X, Wang Y, Wang M. CD70 regulates the NF1/Ras/ERK axis to promote metastatic potential in clear cell renal cell carcinoma. Cancer Cell Int. 2026 26(1):188 10.1186/s12935-026-04277-4"],"submitter_affiliation":["Xi’an Jiaotong-Liverpool University"],"submitter_country":["China"],"pubmed_abstract":["<h4>Background</h4>Despite significant advances in the treatment of clear cell renal cell carcinoma (ccRCC) over the past two decades, therapeutic intervention for patients at advanced or metastatic stages remains a clinical hurdle. Emerging evidence highlights aberrant CD70 expression during tumor progression, supporting its potential as a therapeutic target in advanced ccRCC. However, the molecular mechanisms underlying CD70-mediated metastatic processes remain poorly defined.<h4>Methods</h4>CD70 was knocked out or overexpressed in three ccRCC cell lines, and its role in tumor progression was assessed using in vitro migration and invasion assays, as well as in vivo tumorigenesis and metastasis models. Mass spectrometry-based proteomics was performed to identify differentially expressed proteins and potential pathway dysregulation following CD70 depletion. Co-immunoprecipitation (Co-IP) assays confirmed the CD70-NF1 interaction, and NF1 knockdown in CD70-knockout cells was conducted to reverse the effects of CD70 depletion on Ras/ERK signaling, migration, invasion, and epithelial-mesenchymal transition (EMT)-related features. Expression of EMT-related marks were evaluated by quantitative real-time PCR (qRT-PCR), Western blot, and immunohistochemistry (IHC).<h4>Results</h4>CD70 was significantly upregulated in ccRCC tissues and correlated with poor survival outcomes. CD70 knockout markedly inhibited in vitro cell migration and invasion, as well as in vivo tumor growth and metastasis. Mechanistically, CD70 depletion was associated with increased neurofibromin 1 (NF1) expression in ccRCC cells; CD70 knockout resulted in robust NF1 induction, which in turn suppressed Ras/ERK signaling and downstream EMT-related molecular alterations. Notably, NF1 knockdown largely reversed the inhibitory effects of CD70 knockout on these key molecular and functional phenotype changes.<h4>Conclusions</h4>Our findings uncover a novel CD70-NF1-Ras/ERK axis that contributes to ccRCC progression and metastasis, involving suppression of NF1 and subsequent activation of the Ras/ERK signaling pathway, which further promotes EMT and enhances metastatic capacity. These insights provide a mechanistic foundation for targeting CD70 as a potential therapeutic strategy in advanced ccRCC. Notably, we propose that CD70-targeted therapy may be more effective when combined with agents blocking adaptive escape pathways (e.g., Ras/ERK inhibitors), a hypothesis generated by mechanistic rescue and pharmacologic inhibition in vitro, which require further preclinical validation to confirm synergistic efficacy and clinical viability."],"pubmed_title":["CD70 regulates the NF1/Ras/ERK axis to promote metastatic potential in clear cell renal cell carcinoma."],"pubmed_authors":["Ni Jie J, Gao Aidi A, Chen Ying Y, He Chao C, Wang Xixi X, Savelyeva Natalia N, Dong Xin X, Wang Yiqiang Y, Wang Mu M"],"additional_accession":[]},"is_claimable":false,"name":"CD70 Regulates the NF1/Ras/ERK Axis to Promote Metastatic Potential in Clear Cell Renal Cell Carcinoma","description":"This study is the first report demonstrating a novel mechanism by which CD70 promotes clear cell renal cell carcinoma (ccRCC) progression and metastasis, at least in part, through suppression of NF1 and subsequent activation of the Ras/ERK signaling pathway, which may further drive EMT-related features and enhance tumor metastatic potential. These insights provide a mechanistic rationale for targeting CD70, either alone or in combination with inhibitors of the Ras/ERK pathway or modulators of EMT, to impede metastasis in patients with advanced 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