ArticleNature communications2023
SMARCB1 regulates a TFCP2L1-MYC transcriptional switch promoting renal medullary carcinoma transformation and ferroptosis resistance.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- Methylation profile of individuals with sickle cell trait.Epigenetics · 2025Pooled it
- The roles of chromatin remodeling and 3D genome organization in cancers: from mechanistic insights to emerging treatment options.Molecular cancer · 2026Review
- Whole Blood Transcriptomic Analysis of Sickle Cell Trait.European journal of haematology · 2026Article
- Ferroptosis in renal cell carcinoma: integrative multi-omics insights and therapeutic perspectives.International journal of surgery (London, England) · 2026Article
- Integrated multi-omics analysis revealed that SMARCAL1 serves as an immune related prognostic marker and promotes liver cancer growth via the Hippo/YAP signaling axis.International journal of surgery (London, England) · 2025Article
- Molecular and therapeutic landscape of non-clear cell renal carcinoma.Nature reviews. Urology · 2025Review
- Renal cell carcinoma organoids for precision medicine: bridging the gap between models and patients.Journal of translational medicine · 2025Review
- Single-cell sequencing technology in renal cancer: insights into tumor biology and clinical application.Biomarker research · 2025Review
- Regulation of ferroptosis by transcription factor E2F1.Biochimie · 2025Article
- Tfcp2l1 as a central integrator of hypoxia, dedifferentiation, and tumor progression.Journal of experimental & clinical cancer research : CR · 2025Review
- Beyond the Limit: MYC Mediates Tumor Immune Escape.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Article
- circASAP1 induces renal clear cell carcinoma ferroptosis by binding to HNRNPC and thereby regulating GPX4.Molecular cancer · 2025Article
- TFCP2L1 drives stemness and enhances their resistance to Sorafenib treatment by modulating the NANOG/STAT3 pathway in hepatocellular carcinoma.Oncogenesis · 2024Article
- Ferroptosis in health and disease.Redox biology · 2024Review
- Ferroptosis and cuproptposis in kidney Diseases: dysfunction of cell metabolism.Apoptosis : an international journal on programmed cell death · 2024Review
- Therapeutic Role of Synthetic Lethality inJournal of immunotherapy and precision oncology · 2024Review
- Ferroptosis as an emerging target in sickle cell disease.Current research in toxicology · 2024Article
- Critical role of non-coding RNA-mediated ferroptosis in urologic malignancies.Frontiers in immunology · 2024Review
- Bone-targeting exosome nanoparticles activate Keap1 / Nrf2 / GPX4 signaling pathway to induce ferroptosis in osteosarcoma cells.Journal of nanobiotechnology · 2023Article
Corrections and comments
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Authors and funding
24 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Renal medullary carcinoma (RMC) is an aggressive tumour driven by bi-allelic loss of SMARCB1 and tightly associated with sickle cell trait. However, the cell-of-origin and oncogenic mechanism remain poorly understood. Using single-cell sequencing of human RMC, we defined transformation of thick ascending limb (TAL) cells into an epithelial-mesenchymal gradient of RMC cells associated with loss of renal epithelial transcription factors TFCP2L1, HOXB9 and MITF and gain of MYC and NFE2L2-associated oncogenic and ferroptosis resistance programs. We describe the molecular basis for this transcriptional switch that is reversed by SMARCB1 re-expression repressing the oncogenic and ferroptosis resistance programs leading to ferroptotic cell death. Ferroptosis resistance links TAL cell survival with the high extracellular medullar iron concentrations associated with sickle cell trait, an environment propitious to the mutagenic events associated with RMC development. This unique environment may explain why RMC is the only SMARCB1-deficient tumour arising from epithelial cells, differentiating RMC from rhabdoid tumours arising from neural crest cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.