ArticleEMBO molecular medicine2023
TFEB and TFE3 drive kidney cystogenesis and tumorigenesis.
Article in EMBO molecular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 55 citations in OpenAlex.
- TFEB promotes the progression of t(6; 11) translocation renal cell carcinoma by upregulating LINC00612 expression.Medical oncology (Northwood, London, England) · 2026Article
- Noncanonical mTORC1-TFEB activation promotes hepatocyte plasticity and high-grade malignancy in hepatocellular carcinoma.The Journal of clinical investigation · 2026Article
- Synergistic role of TFEB/TFE3 and mTORC1 in kidney cystogenesis and tumorigenesis.Cell death and differentiation · 2026Article
- Aggressive high-grade papillary-patterned renal cell carcinomas harboring FLCN mutations: expanding the clinicopathological spectrum in Birt-Hogg-Dubé syndrome and sporadic cases.Virchows Archiv : an international journal of pathology · 2026Article
- SPOP-mediated ZMYND8 ubiquitination and phase separation exclusion drives mTOR inhibitor resistance in kidney cancer.Nature communications · 2026Article
- GPNMB-directed CAR T cell therapy against MiT/TFE-family fusion-driven solid tumors.Nature cancer · 2026Article
- Diagnostic utility of novel marker TRIM63 ISH in the workup of uterine perivascular epithelioid cell tumors.Virchows Archiv : an international journal of pathology · 2026Article
- Parotid Oncocytomas Express the Glycoprotein Non-metastatic Melanoma Protein B (GPNMB): A Potential Link with Birt-Hogg-Dubé Syndrome.Head and neck pathology · 2026Article
- Integrated Molecular, Genomic, and Clinical Characterization of Pediatric and Adolescent Translocation Renal Cell Carcinoma: A Report from the Children's Oncology Group.Biomedicines · 2026Article
- Review
- Control of lysosome function by the GTPase-activating protein TBC1D9B and its binding partner TMEM55B.Nature communications · 2026Article
- FLCN loss is characterized by SQSTM1/p62 accumulation despite functional autophagy flux in Birt-Hogg-Dubé syndrome-associated kidney cancer.Autophagy reports · 2026Article
- Substrate-selective mTORC1 regulation and gene dosage-dependent tissue divergence in Birt-Hogg-Dubé syndrome.Frontiers in oncology · 2026Review
- The therapeutic potential of botanicals: how medicinal plants targeting autophagy can reverse metabolic-associated fatty liver disease.Frontiers in pharmacology · 2026Review
- RNA-mediated condensation of TFE3 oncofusions facilitates transcriptional hub formation to promote translocation renal cell carcinoma.Nature communications · 2025Article
- Folliculin Deletion in the Mouse Kidney Results in Cystogenesis of the Loops of Henle via Aberrant TFEB Activation.The American journal of pathology · 2025Article
- Folliculin depletion results in liver cell damage and cholangiocarcinoma through MiT/TFE activation.Cell death and differentiation · 2025Article
- Decoding the dual role of autophagy in cancer through transcriptional and epigenetic regulation.FEBS letters · 2025Review
- Successful treatment of advanced Birt-Hogg-Dubé syndrome-associated renal cell carcinoma with sarcomatoid dedifferentiation using anlotinib combined with PD-1 inhibitor after first-line therapy failure: a case report.World journal of surgical oncology · 2025Article
- Physiologic mechanisms underlying polycystic kidney disease.Physiological reviews · 2025Review
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Authors and funding
23 authors at 7 institutions in 2 countries.
Funding
Abstract
Birt-Hogg-Dubé (BHD) syndrome is an inherited familial cancer syndrome characterized by the development of cutaneous lesions, pulmonary cysts, renal tumors and cysts and caused by loss-of-function pathogenic variants in the gene encoding the tumor-suppressor protein folliculin (FLCN). FLCN acts as a negative regulator of TFEB and TFE3 transcription factors, master controllers of lysosomal biogenesis and autophagy, by enabling their phosphorylation by the mechanistic Target Of Rapamycin Complex 1 (mTORC1). We have previously shown that deletion of Tfeb rescued the renal cystic phenotype of kidney-specific Flcn KO mice. Using Flcn/Tfeb/Tfe3 double and triple KO mice, we now show that both Tfeb and Tfe3 contribute, in a differential and cooperative manner, to kidney cystogenesis. Remarkably, the analysis of BHD patient-derived tumor samples revealed increased activation of TFEB/TFE3-mediated transcriptional program and silencing either of the two genes rescued tumorigenesis in human BHD renal tumor cell line-derived xenografts (CDXs). Our findings demonstrate in disease-relevant models that both TFEB and TFE3 are key drivers of renal tumorigenesis and suggest novel therapeutic strategies based on the inhibition of these transcription factors.
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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.