Project description:TFE3 is a bHLH-ZIP transcription factor, which nuclear localization is regulated by a tumor suppressor FLCN. In order to analyze TFE3 occupancy in whole genome, we have generated and utilized a HK-2 HA-TFE3-inducible cell line which express HA-tagged TFE3 in a doxycycline-dependent manner. HA-TFE3 bound regions were determined by ChIPSeq.
Project description:PSF-TFE3 is an oncogenic chimeric transcription factor derived from human TFE3-rearranged renal cell carcinoma. To analyze its genome-wide occupancy, we developed HA-tagged PSF-TFE3-inducible HK-2 cell lines, which expresses HA-tagged PSF-TFE3 in a doxycycline-dependent manner. We determined the binding regions of HA-PSF-TFE3 by ChIPSeq.
Project description:PRCC-TFE3 is an oncogenic chimeric transcription factor derived from human TFE3-rearranged renal cell carcinoma. To analyze its genome-wide occupancy, we developed HA-tagged PRCC-TFE3-inducible HK-2 cell lines, which expresses HA-tagged TFE3 in a doxycycline-dependent manner. We determined the binding regions of HA-PRCC-TFE3 by ChIPSeq.
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.
Project description:PRCC-TFE3 is an oncogenic chimeric transcription factor that drives TFE3-rearranged renal cell carcinoma. Although PRCC-TFE3 can trigger either oncogene-induced senescence (OIS) or tumor progression depending on the cellular context, both phenotypes are fundamentally dependent on its transcriptional function. This study aims to identify genetic factors essential for the transcriptional activity and functional output of PRCC-TFE3. Using a doxycycline (Dox)-inducible PRCC-TFE3 HK-2 cell model where the fusion protein induces robust OIS, we performed a genome-wide CRISPR/Cas9 knockout screen. By identifying genes whose loss alleviates this OIS phenotype, we sought to uncover key regulators required for PRCC-TFE3-mediated transcriptional programs.
Project description:PRCC-TFE3 is an oncogenic chimeric transcription factor identified in TFE3-rearranged renal cell carcinoma. To characterize PRCC-TFE3–dependent transcriptional programs and their regulation by the Mediator kinase module, we performed RNA sequencing in a doxycycline-inducible PRCC-TFE3 expression system. HK-2 cells expressing HA-tagged PRCC-TFE3 under doxycycline control were cultured under four conditions defined by the presence or absence of doxycycline and the CDK8/19 inhibitor MSC2530818. RNA-seq was conducted to assess global gene expression changes associated with PRCC-TFE3 induction and CDK8/19 inhibition. These data provide a resource for analyzing PRCC-TFE3–driven transcriptional reprogramming and its modulation by the Cyclin C–CDK8/19 Mediator kinase module.
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 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 .