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Figure 1 — TFE3-Rearranged and TFEB-Altered Renal Cell Carcinomas: Molecular Landscape and
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Created: 2026-04-21T18:29:40
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ID: paper-fig-paper-41899560-1
Figure 1Figure 1
Integrated mechanistic model of MiT-RCC driven by TFE3 and TFEB alterations. In TFE3 -rearranged RCC, most fusions join a 5′ partner gene to the 3′ portion of TFE3 , preserving the C-terminal DNA-binding and dimerization domains and promoting constitutive nuclear activity; TFEB -rearranged tumors are driven by analogous transcriptional deregulation, whereas TFEB -amplified RCC is biologically distinct. These events activate a core MiT/TFE transcriptional program that rewires tumor cell metabolism and stress-adaptation pathways. In fusion-driven translocation RCC (tRCC), TFE3 / TFEB fusions induce upregulation of PPARGC1A (PGC-1α), promoting mitochondrial biogenesis and increased dependency on oxidative phosphorylation (OXPHOS), which creates context-specific metabolic vulnerabilities. In parallel, sustained activation of the mTOR-lysosome axis enhances lysosomal biogenesis and autophagy, supporting tumor survival under metabolic stress and reflecting partial uncoupling of M
▸Metadata
| pmid | paper-41899560 |
| caption | Integrated mechanistic model of MiT-RCC driven by TFE3 and TFEB alterations. In TFE3 -rearranged RCC, most fusions join a 5′ partner gene to the 3′ portion of TFE3 , preserving the C-terminal DN |
| image_url | https://www.ebi.ac.uk/europepmc/articles/PMC13025244/bin/cancers-18-00958-g001.jpg |
| paper_title | TFE3-Rearranged and TFEB-Altered Renal Cell Carcinomas: Molecular Landscape and Therapeutic Advances. |
| figure_label | Figure 1 |
| figure_number | 1 |
| _schema_version | 1 |
| source_strategy | pmc_api |
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