ArticleJournal of experimental & clinical cancer research : CR2019
TFE3 fusions escape from controlling of mTOR signaling pathway and accumulate in the nucleus promoting genes expression in Xp11.2 translocation renal cell carcinomas.
Article in Journal of experimental & clinical cancer research : CR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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25 citing papers in PubMed, 78 citations in OpenAlex.
- Review
- TFE3 fusion proteins promoted the progression of Xp11.2 translocation renal cell carcinoma through post-translational modification of PDL1 by upregulating CCND1/Cyclin D1.Cellular oncology (Dordrecht, Netherlands) · 2025Article
- NMRK2 leads to the depletion of CD8Oncogene · 2025Article
- RNA-mediated condensation of TFE3 oncofusions facilitates transcriptional hub formation to promote translocation renal cell carcinoma.Nature communications · 2025Article
- Article
- D-mannose suppresses the angiogenesis and progression of colorectal cancer.Acta biochimica et biophysica Sinica · 2025Article
- Upregulation of GSTP1 mediated by chimeric TFE3 promotes TFE3-tRCC progression by targeting JNK signaling pathway.World journal of surgical oncology · 2024Article
- Comprehensive molecular characterization of TFE3-rearranged renal cell carcinoma.Experimental & molecular medicine · 2024Article
- D-mannose induces TFE3-dependent lysosomal degradation of EGFR and inhibits the progression of NSCLC.Oncogene · 2023Article
- LncRNA like NMRK2 mRNA functions as a key molecular scaffold to enhance mitochondrial respiration of NONO-TFE3 rearranged renal cell carcinoma in an NADJournal of experimental & clinical cancer research : CR · 2023Article
- NOTCH3 missense mutations as predictor of long-term response to gemcitabine in a patient with epithelioid hemangioendothelioma.Journal of cancer research and clinical oncology · 2023Review
- A rare metastatic mesenteric malignant PEComa with TSC2 mutation treated with palliative surgical resection and nab-sirolimus: a case report.Diagnostic pathology · 2023Article
- The Role of Phase-Separated Condensates in Fusion Oncoprotein-Driven Cancers.Annual review of cancer biology · 2023Article
- Emerging roles of TFE3 in metabolic regulation.Cell death discovery · 2023Review
- 5mC and H3K9me3 of TRAF3IP2 promoter region accelerates the progression of translocation renal cell carcinoma.Biomarker research · 2022Article
- Both SUMOylation and ubiquitination of TFE3 fusion protein regulated by androgen receptor are the potential target in the therapy of Xp11.2 translocation renal cell carcinoma.Clinical and translational medicine · 2022Article
- Production and Stabilization of Specific Upregulated Long Noncoding RNA HOXD-AS2 in Glioblastomas Are Mediated by TFE3 and miR-661, Respectively.International journal of molecular sciences · 2022Article
- CircMET promotes tumor proliferation by enhancing CDKN2A mRNA decay and upregulating SMAD3.Molecular cancer · 2022Article
- Autophagy in Xp11 translocation renal cell carcinoma: from bench to bedside.Molecular and cellular biochemistry · 2021Review
- Estradiol increases risk of topoisomerase IIβ-mediated DNA strand breaks to initiate Xp11.2 translocation renal cell carcinoma.Cell communication and signaling : CCS · 2021Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundXp11.2 translocation renal cell carcinoma (tRCC) is mainly caused by translocation of the TFE3 gene located on chromosome Xp11.2 and is characterized by overexpression of the TFE3 fusion gene. Patients are diagnosed with tRCC usually before 45 years of age with poor prognosis. We investigated this disease using two tRCC cell lines, UOK109 and UOK120, in this study.
methodsThe purpose of this study was to investigate the pathogenic mechanism of TFE3 fusions in tRCC based on its subcellular localization, nuclear translocation and transcriptional activity. The expression of TFE3 fusions and other related genes were analyzed by quantitative reverse transcription PCR (qRT-PCR) and Western blot. The subcellular localization of TFE3 was determined using immunofluorescence. The transcriptional activity of TFE3 fusions was measured using a luciferase reporter assay and ChIP analysis. In some experiments, TFE3 fusions were depleted by RNAi or gene knockdown. The TFE3 fusion segments were cloned into a plasmid expression system for expression in cells.
resultsOur results demonstrated that TFE3 fusions were overexpressed in tRCC with a strong nuclear retention irrespective of treatment with an mTORC1 inhibitor or not. TFE3 fusions lost its co-localization with lysosomal proteins and decreased its interaction with the chaperone 14-3-3 proteins in UOK109 and UOK120 cells. However, the fusion segments of TFE3 could not translocate to the nucleus and inhibition of Gsk3β could increase the cytoplasmic retention of TFE3 fusions. Both the luciferase reporter assay and ChIP analysis demonstrated that TFE3 fusions could bind to the promoters of the target genes as a wild-type TFE3 protein. Knockdown of TFE3 results in decreased expression of those genes responsible for lysosomal biogenesis and other target genes. The ChIP-seq data further verified that, in addition to lysosomal genes, TFE3 fusions could regulate genes involved in cellular responses to hypoxic stress and transcription.
conclusionsOur results indicated that the overexpressed TFE3 fusions were capable of escaping from the control by the mTOR signaling pathway and were accumulated in the nucleus in UOK109 and UOK120 cells. The nuclear retention of TFE3 fusions promoted the expression of lysosomal genes and other target genes, facilitating cancer cell resistance against an extreme environment.
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