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Gene expression changes induced by HA-PRCC-TFE3 in HEK293 cells

ABSTRACT: PRCC-TFE3 is an oncogenic chimeric transcription factor identified in human TFE3-rearranged renal cell carcinoma. To analyze gene expression changes driven by PRCC-TFE3, we generated and utilized an HA-tagged PRCC-TFE3-inducible HEK293 cell line, which expresses HA-tagged PRCC-TFE3 in a doxycycline-dependent manner. Cells were cultured with or without doxycycline, and comprehensive gene expression analysis was conducted using Affymetrix arrays .

ORGANISM(S): Homo sapiens

PROVIDER: GSE281146 | GEO | 2025/01/07

REPOSITORIES: GEO

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Gene expression changes induced by HA-PRCC-TFE3 in HK-2 cells

Project description:PRCC-TFE3 is an oncogenic chimeric transcription factor identified in human TFE3-rearranged renal cell carcinoma. To analyze gene expression changes driven by PRCC-TFE3, we generated and utilized an HA-tagged PRCC-TFE3-inducible HK-2 cell line, which expresses HA-tagged PRCC-TFE3 in a doxycycline-dependent manner. Cells were cultured with or without doxycycline, and comprehensive gene expression analysis was conducted using RNA-seq.

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PRCC-TFE3 Function and the Role of HIF1α and HIF2α in TFE3-Rearranged Renal Cell Carcinoma Development

Project description:PRCC-TFE3 is an oncogenic chimeric transcription factor identified in human TFE3-rearranged renal cell carcinoma. To investigate the function of PRCC-TFE3 in vivo, we generated PRCC-TFE3 knock-in (KI) mice by inserting a loxP-STOP-loxP-PRCC-TFE3 cassette into the Rosa26 locus. When PRCC-TFE3 KI mice were crossed with Cadherin 16-Cre transgenic mice (KSP-Cre), the resulting mice developed TFE3-RCC in the kidney. Our findings revealed that hypoxia-inducible factors HIF1α and HIF2α are directly upregulated by PRCC-TFE3. To clarify the roles of HIF1α and HIF2α in TFE3-RCC development, we further crossed PRCC-TFE3 KI mice with HIF1α flox and/or HIF2α flox mice.

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Project description:TFE3 (transcription factor binding to IGHM enhancer 3) nuclear translocation and transcriptional activity has been implicated in PINK1-PRKN/parkin-dependent mitophagy. However, the transcriptional control governing the mitophagy in TFE3/Xp11.2 translocation renal cell carcinoma (TFE3 tRCC) is largely unknown. Here, we investigated the role and mechanisms of PRCC-TFE3 fusion protein, one of TFE3 fusion types in TFE3 tRCC, in governing mitophagy to promote development of PRCC-TFE3 tRCC. We observed and analyzed mitophagy, transcriptional control of PRCC-TFE3 on PINK1-PRKN-dependent mitophagy, PRCC-TFE3 fusions nuclear translocation, cancer cell survival and proliferation under mitochondrial oxidative damage in PRCC-TFE3 tRCC cell line. We found that nuclear-aggregated PRCC-TFE3 fusions constitutively activated expression of the target gene E3 ubiquitin ligase PRKN, leading to rapid PINK1-PRKN-dependent mitophagy that promoted cell survival under mitochondrial oxidative damage as well as cell proliferation through decreasing mitochondrial ROS formation. However, nuclear translocation of TFE3 fusions escaped from PINK1-PRKN-dependent mitophagy. Furthermore, we confirmed that PRCC-TFE3 fusion accelerated mitochondrial turnover by activating PPARGC1A/PGC1α-NRF1. In conclusion, our findings indicated a major role of PRCC-TFE3 fusion-mediated mitophagy and mitochondrial biogenesis in promoting proliferation of PRCC-TFE3 tRCC.

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