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GCN2 enhances the growth and progression of prostate cancer by maintaining amino acid homeostasis [mRNA-seq]

ABSTRACT: Here we report mRNA seq on DMSO and GCN2iB treated WT LNCaP cells

ORGANISM(S): Homo sapiens

PROVIDER: GSE196252 | GEO | 2022/10/17

REPOSITORIES: GEO

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GCN2 enhances the growth and progression of prostate cancer by maintaining amino acid homeostasis [CHARGE-seq]

Project description:Here we report genome wide tRNA charging analysis (CHARGE seq) on DMSO, GCN2iB and GCN2iB plus essential amino acid (EAA) treated WT LNCaP cells

2022-10-17 | GSE196251 | GEO

GCN2 enhances the growth and progression of prostate cancer by maintaining amino acid homeostasis

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

2022-10-18 | GSE196253 | GEO

GCN2 enhances the growth and progression of prostate cancer by maintaining amino acid homeostasis

Project description:GCN2 enhances the growth and progression of prostate cancer by maintaining amino acid homeostasis

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GCN2 enhances the growth and progression of prostate cancer by maintaining amino acid homeostasis [mRNA-seq]

Project description:GCN2 enhances the growth and progression of prostate cancer by maintaining amino acid homeostasis [mRNA-seq]

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GCN2 enhances the growth and progression of prostate cancer by maintaining amino acid homeostasis [CHARGE-seq]

Project description:GCN2 enhances the growth and progression of prostate cancer by maintaining amino acid homeostasis [CHARGE-seq]

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Autophagy contributes to sulfonylurea herbicide tolerance via GCN2-independent regulation of amino acid homeostasis.

Project description:Sulfonylurea (SU) herbicides inhibit branched-chain amino acid (BCAA) biosynthesis by targeting acetolactate synthase. Plants have evolved target-site resistance and metabolic tolerance to SU herbicides; the GCN2 (general control non-repressible 2) pathway is also involved in SU tolerance. Here, we report a novel SU tolerance mechanism, autophagy, which we call 'homeostatic tolerance,' is involved in amino acid signaling in Arabidopsis. The activation and reversion of autophagy and GCN2 by the SU herbicide tribenuron-methyl (TM) and exogenous BCAA, respectively, confirmed that TM-induced BCAA starvation is responsible for the activation of autophagy and GCN2. Genetic and biochemical analyses revealed a lower proportion of free BCAA and more sensitive phenotypes in atg5, atg7, and gcn2 single mutants than in wild-type seedlings after TM treatment; the lowest proportion of free BCAA and the most sensitive phenotypes were found in atg5 gcn2 and atg7 gcn2 double mutants. Immunoblotting and microscopy revealed that TM-induced activation of autophagy and GCN2 signaling do not depend on the presence of each other, and these 2 pathways may serve as mutually compensatory mechanisms against TM. TM inhibited the TOR (target of rapamycin), and activated autophagy in an estradiol-induced TOR RNAi line, suggesting that TM-induced BCAA starvation activates autophagy, probably via TOR inactivation. Autophagy and GCN2 were also activated, and independently contributed to TM tolerance in plants conferring metabolic tolerance. Together, these data suggest that autophagy is a proteolytic process for amino acid recycling and contributes to GCN2-independent SU tolerance, probably by its ability to replenish fresh BCAA.

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Gene expression analysis of prostate cancer cells treated with fatty acid synthase (FASN) inhibitor IPI-9119

Project description:Alterations in gene expression following fatty acid synthase inhibtion were evaluated in androgen sensitive LNCaP cells and castration resistant 22Rv1 and LNCaP-95 cells. Cell were exposed to 2 concentrations (0.1 and 0.5 uM) of FASN inhibitor IPI-9119 or DMSO for 6 days.

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Amino acid sensor GCN2 promotes SARS-CoV-2 receptor ACE2 expression in response to amino acid deprivation.

Project description:Angiotensin-converting enzyme 2 (ACE2) has been identified as a primary receptor for severe acute respiratory syndrome coronaviruses 2 (SARS-CoV-2). Here, we investigated the expression regulation of ACE2 in enterocytes under amino acid deprivation conditions. In this study, we found that ACE2 expression was upregulated upon all or single essential amino acid deprivation in human colonic epithelial CCD841 cells. Furthermore, we found that knockdown of general control nonderepressible 2 (GCN2) reduced intestinal ACE2 mRNA and protein levels in vitro and in vivo. Consistently, we revealed two GCN2 inhibitors, GCN2iB and GCN2-IN-1, downregulated ACE2 protein expression in CCD841 cells. Moreover, we found that increased ACE2 expression in response to leucine deprivation was GCN2 dependent. Through RNA-sequencing analysis, we identified two transcription factors, MAFB and MAFF, positively regulated ACE2 expression under leucine deprivation in CCD841 cells. These findings demonstrate that amino acid deficiency increases ACE2 expression and thereby likely aggravates intestinal SARS-CoV-2 infection.

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GCN2 sustains mTORC1 suppression upon amino acid deprivation by inducing Sestrin2.

Project description:Mammalian cells possess two amino acid-sensing kinases: general control nonderepressible 2 (GCN2) and mechanistic target of rapamycin complex 1 (mTORC1). Their combined effects orchestrate cellular adaptation to amino acid levels, but how their activities are coordinated remains poorly understood. Here, we demonstrate an important link between GCN2 and mTORC1 signaling. Upon deprivation of various amino acids, activated GCN2 up-regulates ATF4 to induce expression of the stress response protein Sestrin2, which is required to sustain repression of mTORC1 by blocking its lysosomal localization. Moreover, Sestrin2 induction is necessary for cell survival during glutamine deprivation, indicating that Sestrin2 is a critical effector of GCN2 signaling that regulates amino acid homeostasis through mTORC1 suppression.

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Project description:Analysis of prostate adnocarcinoma cell line LNCaP cells overexpression pair box 5 (PAX5) for up to 4 days. The goals of this study are to compare PAX5 overexpression in LNCaP cell drives transcriptome profiling (RNA-seq) changes.

2021-01-31 | GSE129887 | GEO

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