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The effect of TCOF1 on renal cancer proteome

ABSTRACT: TCOF1 encodes treacle, a multifunctional protein involved in ribosome biogenesis, regulation of mitosis, proliferation, response to DNA damage, and apoptosis. TCOF1 mutations cause Treacher Collins syndrome, a rare genetic disorder leading to craniofacial malformations. The expression of TCOF1 is disturbed in renal cancer. The global effects of TCOF1 dysfunction in cancer are unknown. Here, we explored the effect of TCOF1 depletion on proteome of renal cancer.

INSTRUMENT(S):

ORGANISM(S): Rattus Norvegicus (rat)

SUBMITTER: Jacek Wisniewski

LAB HEAD: Jacek R Wisniewski

PROVIDER: PXD027601 | Pride | 2026-05-25

REPOSITORIES: Pride

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	20210621_EXPL3_JRW_SA_L_XX21.raw	Raw
	20210621_EXPL3_JRW_SA_L_XX22.raw	Raw
	20210621_EXPL3_JRW_SA_L_XX23.raw	Raw
	20210621_EXPL3_JRW_SA_L_XX24.raw	Raw
	20210621_EXPL3_JRW_SA_L_XX25.raw	Raw

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Publications

TCOF1 affects Golgi secretory pathway contributing to the angiogenesis in renal cancer.

Grzanka Małgorzata M Popławski Piotr P Wiśniewski Jacek R JR Iwanicka-Nowicka Roksana R Kossowska Helena H Koblowska Marta M Rybicka Beata B Białas Alex A Piekiełko-Witkowska Agnieszka A

Cell communication and signaling : CCS 20260317 1

BACKGROUND: TCOF1 is a nucleolar protein involved in ribosome biogenesis, DNA damage response, and mitotic regulation. Germline TCOF1 mutations are associated with Treacher-Collins syndrome, a rare congenital disorder characterized by craniofacial abnormalities. Clear cell renal cell carcinoma (ccRCC), the most prevalent form of kidney cancer, exhibits pronounced nuclear and nucleolar pleomorphism, which correlates with tumour aggressiveness. The ccRCC grading system relies on microscopic evalua ...[more]

PMID: 41840584

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TCOF1 DRIVES STEMNESS OF TRIPLE-NEGATIVE BREAST CANCER THROUGH KIT

Project description:Triple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer with poor prognosis. The high malignancy of TNBC is contributed by its heterogeneity and enrichment of cancer stem cells. By performing multiomic profiling, we recently uncovered super-enhancer heterogeneity between breast cancer subtypes. Here, we identify TCOF1 as a novel super-enhancer-regulated gene that promotes TNBC growth and stemness. TCOF1, which plays a critical role in craniofacial development, is frequently upregulated in TNBC and its elevated expression correlates with shorter overall survival. Whereas TCOF1 depletion has potent effects on the growth and stemness of basal-like TNBC, it has no effect on mesenchymal-like cells, highlighting the distinct molecular dependency in different subgroups of TNBC. Whole genome RNA sequencing uncovers several stem cell molecules regulated by TCOF1. We further demonstrate that the upregulation of KIT by TCOF1 mediates TNBC stemness. These findings provide a rationale for developing therapeutics targeting TCOF1 in basal-like TNBC.

2021-11-02 | GSE168835 | GEO

The effect of TCOF1 silencing in renal cancer cells

Project description:TCOF1 is a nucleolar protein involved in ribosome biogenesis, response to DNA damage and oxidative stress. Clear cell renal cell cancer (ccRCC) is characterized by pronounced nucleolar pleomorphism which is utilized in the ccRCC tumor grading system. Here, we hypothesized that TCOF1 may contribute to the tumorigenesis of ccRCC. To explore the impact of TCOF1 on ccRCC, we silenced its expression in ccRCC cells and analyzed their transcriptome using microarrays.

2026-05-15 | GSE299580 | GEO

The effect of TCOF1 silencing in renal cancer cells

Project description:The effect of TCOF1 silencing in renal cancer cells

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Proteomic-based analysis of hypoxia and physioxia responsive proteins and pathways in DLBCLProteomic-based analysis of hypoxia and physioxia responsive proteins and pathways in DLBCL

Project description:Hypoxia is damaging to normal cells as well as cancerous cells. Reports assessing hypoxia- and physioxia-induced global proteome changes in lymphoma are lacking. Here, we sought to explore how the proteome of diffuse large B-cell lymphoma (DLBCL) changes when cells are exposed to the acute hypoxic stress (1% of O2) and the physioxia (5% of O2) for a long-time. A total of 8239 proteins were identified by LC-MS/MS, of which 718, 513, and 486 have significant changes in abundance in Ri-1, U2904, and U2932 cell lines, respectively. We observed that changes in B-NHL proteome profiles induced by hypoxia and physioxia were quantitatively similar in each cell line; however, differentially abundant proteins (DAPs) were specific to a certain cell line. A significant down-regulation of several ribosome proteins indicated a translational inhibition of new ribosome protein synthesis in hypoxia, what was confirmed in a pathway enrichment analysis. In addition, down-regulated proteins highlighted the altered cell cycle, metabolism, and interferon signaling. As expected, the enrichment of up-regulated proteins revealed terms related to metabolism, HIF1 signaling, and response to oxidative stress. In accordance to our results, physioxia induced weaker changes in the protein abundance when compared to those induced by hypoxia. Our data provide new evidence for understanding mechanisms by which DLBCL cells respond to a varia-ble oxygen level. Furthermore, this study reveals multiple hypoxia-responsive proteins showing an altered abundance in hypoxic and physioxic DLBCL, potentially important in developing more aggressive phenotype.

2022-02-17 | PXD026726 | Pride

HSP70-driven molecular response to the proteasome machinery inhibition is a vulnerability in cancer

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2025-10-29 | PXD027840 | Pride

Comparison of proteome composition of serum enriched in extracellular vesicles isolated from polycythemia vera patients and healthy controls

Project description:Extracellular vesicles (EVs), e.g., exosomes and microvesicles, are one of the main networks of intercellular communication. In myeloproliferative disorders, such as polycythemia vera (PV), excess of EVs originating from overabundant blood cells can directly contribute to thrombosis through their procoagulant activity. However, proteomic composition of these vesicles in PV patients has not been investigated before. In this work, we examined proteomic composition of serum exosomes of PV patients in comparison to healthy controls. We processed exosome-enriched serum samples using Multiple Enzyme Filter Aided Sample Preparation approach (MED-FASP), conducted LC-MS/MS measurements on a Q-Exactive HF-X mass spectrometer, and quantitatively analyzed the absolute concentrations of identified proteins by Total Protein Approach (TPA). 38 proteins were present at statistically significant different concentrations between PV patients’ study group and healthy controls’ group. The main protein components deregulated in PV were primarily related with excessive amounts of cells (TFRC, SELL, GP5), increased platelet activation (SERPINE1, MMRN1), elevated immune and inflammatory response (HPSE, CAMP, LYZ, SELL, LTF), and high concentrations of procoagulant and angiogenetic agents (ANG, HPSE). Our study provides the first quantitative analysis of the serum exosomes’ proteome in PV patients. Acquired knowledge can be beneficial to understanding of the mechanism of PV disease and further development of diagnostic or therapeutic procedures.

2019-05-13 | PXD013234 | Pride

Human liver cells proteome

Project description:The human liver functions through a complex interplay of parenchymal and non-parenchymal cells, which participate in performing many essential aspects of metabolism and secretion. Mass spectrometry-based proteomic analysis of intact tissue has improved the understanding of these processes, by providing an in-depth view of the human liver proteome. However, the predominance of parenchymal cells, i.e. hepatocytes, means that the total tissue proteome mainly reflects hepatocyte expression. In this study, we therefore used quantitative label-free proteomic analysis to analyze the proteomes of the major parenchymal and non-parenchymal cell types in the human liver, i.e. hepatocytes, liver sinusoidal endothelial cells, Kupffer cells, and hepatic stellate cells. We found that our data recapitulated specific functional differences between cell types, meaning that it can be used to reliably probe various aspects of cellular interplay. Thus, the data we provide constitutes a unique resource for exploring the human liver proteome at major cell type resolution.

2020-04-09 | PXD012615 | Pride

Protein arginine methyltransferase PRMT1 is essential for palatogenesis

Project description:We report that neural crest-specific deletion of Prmt1 caused craniofacial malformations including cleft palate.

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Regulation of Megakaryocytic differentiation in Cell Line Models by Dynamic Combinatorial Interactions of RUNX1 with Its Cooperating Partners

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Cell fate determination by ubiquitin-dependent regulation of translation

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