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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE246790 | GEO | 2024/03/29

REPOSITORIES: GEO

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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

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

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

| PRJNA1034612 | ENA

S1PR3–G12-biased agonist ALESIA targets cancer metabolism and promotes glucose starvation

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

2021-02-08 | GSE143670 | GEO

Protein Kinase A Activation Promotes Cancer Cell Resistance to Glucose Starvation and Anoikis.

Project description:Cancer cells often rely on glycolysis to obtain energy and support anabolic growth. Several studies showed that glycolytic cells are susceptible to cell death when subjected to low glucose availability or to lack of glucose. However, some cancer cells, including glycolytic ones, can efficiently acquire higher tolerance to glucose depletion, leading to their survival and aggressiveness. Although increased resistance to glucose starvation has been shown to be a consequence of signaling pathways and compensatory metabolic routes activation, the full repertoire of the underlying molecular alterations remain elusive. Using omics and computational analyses, we found that cyclic adenosine monophosphate-Protein Kinase A (cAMP-PKA) axis activation is fundamental for cancer cell resistance to glucose starvation and anoikis. Notably, here we show that such a PKA-dependent survival is mediated by parallel activation of autophagy and glutamine utilization that in concert concur to attenuate the endoplasmic reticulum (ER) stress and to sustain cell anabolism. Indeed, the inhibition of PKA-mediated autophagy or glutamine metabolism increased the level of cell death, suggesting that the induction of autophagy and metabolic rewiring by PKA is important for cancer cellular survival under glucose starvation. Importantly, both processes actively participate to cancer cell survival mediated by suspension-activated PKA as well. In addition we identify also a PKA/Src mechanism capable to protect cancer cells from anoikis. Our results reveal for the first time the role of the versatile PKA in cancer cells survival under chronic glucose starvation and anoikis and may be a novel potential target for cancer treatment.

| S-EPMC4792400 | biostudies-literature

The transcription factors TFEB and TFE3 link the FLCN-AMPK signaling axis to innate immune response and pathogen resistance

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

2019-03-08 | GSE126656 | GEO

Ras-induced epigenetic inactivation of RRAD promotes glucose uptake in a human ovarian cancer model

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-08-21 | E-GEOD-55568 | biostudies-arrayexpress

A kidney-hypothalamus axis promotes compensatory glucose production in response to glycosuria.

Project description:The kidneys facilitate energy conservation through reabsorption of nutrients including glucose. Almost all of the filtered blood glucose is reabsorbed by the kidneys. Loss of glucose in urine (glycosuria) is offset by an increase in endogenous glucose production to maintain normal energy supply in the body. How the body senses this glucose loss and consequently enhances glucose production is unclear. Using renal Glut2 knockout mice, we demonstrate that elevated glycosuria activates the hypothalamic-pituitary-adrenal axis, which in turn drives endogenous glucose production. This phenotype was attenuated by selective afferent renal denervation, indicating the involvement of the afferent nerves in promoting the compensatory increase in glucose production. In addition, through plasma proteomics analyses we observed that acute phase proteins - which are usually involved in body's defense mechanisms against a threat - were the top candidates which were either upregulated or downregulated in renal Glut2 KO mice. Overall, afferent renal nerves contribute to promoting endogenous glucose production in response to elevated glycosuria and loss of glucose in urine is sensed as a biological threat in mice. These findings may be useful in improving efficiency of drugs like SGLT2 inhibitors that are intended to treat hyperglycemia by enhancing glycosuria, but are met with a compensatory increase in endogenous glucose production.

| S-EPMC10542134 | biostudies-literature

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