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TFE3-SLC36A1 axis promotes resistance to glucose starvation in kidney cancer cells [ChIP-Seq]

ABSTRACT: TFE3-SLC36A1 axis promotes resistance to glucose starvation in kidney cancer cells [ChIP-Seq]

PROVIDER: PRJNA1034612 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26631152_1.fastq.gz	Fastqsanger.gz
	SRR26631152_2.fastq.gz	Fastqsanger.gz
	SRR26631153_1.fastq.gz	Fastqsanger.gz
	SRR26631153_2.fastq.gz	Fastqsanger.gz
	SRR26631154_1.fastq.gz	Fastqsanger.gz

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TFE3-SLC36A1 axis promotes resistance to glucose starvation in kidney cancer cells [ChIP-Seq]

Project description:"Starving cancer to death" is pursued for cancer therapy. An intriguing regime is to inhibit glucose transporter GLUT1 in cancer cells. But past attempts are challenged by that cancer cells can somehow tolerate starvation. In addition, during cancer progression, cancer cells may suffer from insufficient nutrient supply, for example due to insufficient angiogenesis. So uncovering mechanism of starvation resistance shall not only shed insight into cancer progression but also benefit cancer therapy. TFE3 is known as a transcription factor capable of activating autophagic genes. Physiological TFE3 activity is regulated by phosphorylation-triggered translocation, which is sensitive to nutrient status. We recently reported TFE3 constitutively localizes to cell nucleus in kidney cancer, promoting cell proliferation even under replete condition. But whether and how TFE3 affects kidney cancer cell sensitivity to starvation is unclear. In this study, we find TFE3 promotes kidney cancer cell resistance to glucose starvation. We show starvation triggers TFE3 protein stabilization through increasing its O-GlcNAcylation. Furthermore, through unbiased functional genomic study, we identify genes sensitive to TFE3 protein level, including SLC36A1, a lysosomal amino acid transporter. We find SLC36A1 is overexpressed in kidney cancer, promotes mTOR activity and kidney cancer cell proliferation. Importantly, SLC36A1 level is directly upregulated by TFE3 upon starvation, which enhances cellular resistance to starvation. Suppressing TFE3 or SLC36A1 significantly increased cellular sensitivity to GLUT1 inhibitor in kidney cancers. Collectively, we uncover a TFE3-SLC36A1 axis that responds to starvation and enhances starvation tolerance in kidney cancer.

2024-03-29 | GSE246789 | GEO

TFE3-SLC36A1 axis promotes resistance to glucose starvation in kidney cancer cells [RNA-Seq]

2024-03-29 | GSE246788 | GEO

TFE3-SLC36A1 axis promotes resistance to glucose starvation in kidney cancer cells

Project description:TFE3-SLC36A1 axis promotes resistance to glucose starvation in kidney cancer cells

| PRJNA1034611 | ENA

TFE3-SLC36A1 axis promotes resistance to glucose starvation in kidney cancer cells [RNA-Seq]

Project description:TFE3-SLC36A1 axis promotes resistance to glucose starvation in kidney cancer cells [RNA-Seq]

| PRJNA1034613 | ENA

RNA changes upon glucose starvation

Project description:The adaptation of tumor cells to metabolic stress is crucial for tumor development. We demonstrate that the translation of NRF2, a master regulator of antioxidant response, is controlled by the OGDH-METTL3 axis in melanoma for glucose starvation adaptation. To elucidate the regulatory mechanism of the OGDH-METTL3 axis during glucose starvation, we conducted co-immunoprecipitation and mass spectrometry analysis to identify the binding partner of OGDH that governs both the OGDH-METTL3 axis and tumor cell adaptation to glucose deprivation.

2025-01-01 | GSE252314 | GEO

Transcriptional regulation of FAM134B by TFEB/TFE3 controls ER-phagy in response to starvation and chondrocyte differentiation

Project description:Lysosomal degradation of the endoplasmic reticulum (ER) via autophagy (ER-phagy) is emerging as a critical regulator of cell homeostasis and function1. The recent identification of ER-phagy receptors has shed light on the molecular mechanism underlining this process; however, the signaling pathways regulating ER-phagy in response to cellular needs are still largely unknown. We found that the nutrient responsive transcription factors TFEB and TFE3 - master regulators of lysosomal biogenesis and autophagy2- control ER-phagy by inducing the expression of the ER-phagy receptor FAM134B. The TFEB/TFE3-FAM134B axis promotes ER-phagy activation upon prolonged starvation. In addition, we discovered that this pathway is activated in chondrocytes by FGF signaling, a critical regulator of cell differentiation 3. FGF signaling induces a JNK-dependent proteasomal degradation of the insulin receptor substrate 1, which inhibits the insulin-PI3K-PKB/Akt-mTORC1 pathway and promotes TFEB/TFE3 nuclear translocation and FAM134B induction. Consistent with a role of the TFEB/TFE3-FAM134B axis in chondrocytes, FAM134B knock-down impairs cartilage growth and mineralization in medaka fish. This study identifies a new signaling pathway that allows ER-phagy to respond to both metabolic and developmental cues.

2020-07-15 | PXD015326 | Pride

RNA changes upon glucose starvation

Project description:RNA changes upon glucose starvation

| PRJNA1059633 | ENA

Transcriptional regulation of the innate immune reponse by the MITF/TFE3 family

Project description:To understand the activation of the MITF/TFE transcription factors in effective defense against pathogens we examined the genome wide distribution of TFE3 in control and activated mouse macrophages. It was determined that TFEB and TFE3 collaborate with each other to promote efficient autophagy induction, increased lysosomal biogenesis, and transcriptional upregulation of proinflammatory cytokines and key mediators of the inflammatory response. 4 samples were analyzed: Background Control, Control, Starvation, LPS

2016-02-01 | E-GEOD-75822 | biostudies-arrayexpress

TFE3-SLC36A1 axis promotes resistance to glucose starvation in kidney cancer cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-03-29 | GSE246790 | GEO

Glucose starvation Bacillus subtilis

Project description:Glucose starvation Bacillus subtilis

2010-12-13 | PRD000196 | Pride