Dataset Information

Proteomic analysis of renal cancer secretome

ABSTRACT: Introduction/aim: Renal cell cancer (RCC) is the most frequent kidney malignancy. Here, we aimed to analyze RCC secretome to find key molecules involved in tumor microenvironment regulation. Methods: Conditioned media from five RCC-derived cell lines (Caki-1, KIJ-265T, KIJ-308T, 786-O, and A498) and a non-cancerous proximal tubules (RPTEC) were used for mass spectrometry based proteomic analysis. The results were evaluated using Gene Onthology algorithms. Results: When compared with RPTEC, CM of Caki-1 and KIJ265T contained 587 and 802 aberrantly expressed proteins, respectively. Remarkably, there were 360 proteins commonly found in CM from Caki-1 and KIJ265T cells, with striking 348 proteins with changes in similar directions. 786-O CM expressed 612, A498 569, and KIJ308T 802 proteins. All cell lines shared 124 aberrantly expressed CM proteins, with 119 proteins with changes in the same direction. Top commonly downregulated proteins included SCIN, CBR4, MUC1, PELP1, LSM1, while top upregulated proteins were BZW2, COLGALT1, EEF1A2, CSDE1, INHBA, and STAT1. GO analysis of cellular components related to the identified proteins revealed that 63 proteins were associated with extracellular exosomes. Conclusion: Different RCC cell lines secrete proteins, commonly altered when compared with normal kidney proximal tubules. 53% of these proteins are associated with extracellular exosomes.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (ncbitaxon:9606)

SUBMITTER: Agnieszka Piekielko-Witkowska

PROVIDER: MSV000088490 | MassIVE | Thu Dec 02 03:53:00 GMT 2021

SECONDARY ACCESSION(S): PXD030085

REPOSITORIES: MassIVE

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Publications

Coordinated reprogramming of renal cancer transcriptome, metabolome and secretome associates with immune tumor infiltration.

Poplawski Piotr P Alseekh Saleh S Jankowska Urszula U Skupien-Rabian Bozena B Iwanicka-Nowicka Roksana R Kossowska Helena H Fogtman Anna A Rybicka Beata B Bogusławska Joanna J Adamiok-Ostrowska Anna A Hanusek Karolina K Hanusek Jan J Koblowska Marta M Fernie Alisdair R AR Piekiełko-Witkowska Agnieszka A

Cancer cell international 20230105 1

<h4>Background</h4>Clear cell renal cell carcinoma (ccRCC) is the most common subtype of renal cancer. The molecules (proteins, metabolites) secreted by tumors affect their extracellular milieu to support cancer progression. If secreted in amounts detectable in plasma, these molecules can also serve as useful, minimal invasive biomarkers. The knowledge of ccRCC tumor microenvironment is fragmentary. In particular, the links between ccRCC transcriptome and the composition of extracellular milieu ...[more]

PMID: 36604669

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Project description:Background: Acute kidney injury (AKI) is a common clinical event with high morbidity and mortality. We previously demonstrated that injection of cord blood endothelial colony forming cell (ECFC)-derived exosomes, highly enriched in miRNA(miR)-486-5p, prevented ischemic kidney injury in mice. While preclinical models support involvement of several miRs in AKI, the direct effects of miR-486-5p on injury and the kidney transcriptome are unknown. Objective: We studied effects of miR-486-5p in mice with kidney ischemia-reperfusion (IR) injury, and compared the impact of miR-486-5p and ECFC-derived exosomes on the transcriptome of proximal tubules (PTs) and renal endothelial cells. Methods: Adult male mice were subjected to bilateral kidney ischemia (30 min), and injected via tail vein with or without vehicle, miR-486-5p mimic, ECFC-derived exosomes, or scramble miR at the start of reperfusion. Plasma and tissues were collected 24 hrs after reperfusion, and proximal tubular and endothelial cells were isolated for mRNA analysis by RNA-Seq. Results: In mice with kidney IR, injection of miR-486-5p mimic increased levels of miR-486-5p in proximal tubules and endothelial cells, and significantly improved plasma creatinine, histological injury, neutrophil infiltration, and apoptosis, compared to vehicle treatment. MiR-486-5p inhibited expression of phosphatase and tensin homolog (PTEN), and activated AKT. Similar results were observed with exosomes, but scramble miR had no effect. In proximal tubules, miR-486-5p or exosomes reduced expression of several AKI genes (e.g. Lcn2, Havcr1 and Krt20) and caused alterations in apoptotic genes compared to IR alone. In endothelium, miR-486-5p or exosomes caused milder effect than in PTs but still impacting on expression of injury-related genes. Conclusion: MiR-486-5p protects mice against ischemic kidney injury. Both miR-486-5p and exosomes reduce expression of apoptotic genes in PTs and endothelium. The results suggest that systemic delivery of miR-486-5p has therapeutic potential in ischemic AKI.