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Gene expression profiling of control or TFEB knock out HeLa cell under Wnt3a-CM treatment condition

ABSTRACT: Gene expression profiling of control or TFEB knock out HeLa cell under Wnt3a-CM treatment condition

PROVIDER: PRJNA616332 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11452757_1.fastq.gz	Fastqsanger.gz
	SRR11452757_2.fastq.gz	Fastqsanger.gz
	SRR11452758_1.fastq.gz	Fastqsanger.gz
	SRR11452758_2.fastq.gz	Fastqsanger.gz
	SRR11452759_1.fastq.gz	Fastqsanger.gz

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Gene expression profiling of control or TFEB knock out HeLa cell under Wnt3a-CM treatment condition

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Project description:Birt-Hogg-Dubè (BHD) syndrome is an inherited condition caused by loss-of-function mutations in the gene encoding the tumor-suppressor protein folliculin (FLCN) and frequently associated with kidney cysts and cancer. 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 previously showed 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. Importantly, silencing of either TFEB or TFE3 rescued tumorigenesis in patient-derived xenografts (PDXs) generated from a kidney tumor of a BHD patient. Furthermore, transcriptome analyses performed in transgenic mice, PDXs and patient tumor samples revealed TFEB/TFE3 downstream targets that may contribute to their tumorigenic activity. Our findings demonstrate in disease-relevant models that TFEB and TFE3 are key drivers of kidney tumorigenesis and suggest novel therapeutic strategies based on the inhibition of these transcription factors.

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