Ribosome dynamics following arginine deprivation in colon cancer cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA880902 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21595020.fastq.gz | Fastqsanger.gz | |||
| SRR21595021.fastq.gz | Fastqsanger.gz | |||
| SRR21595022.fastq.gz | Fastqsanger.gz | |||
| SRR21595023.fastq.gz | Fastqsanger.gz | |||
| SRR21595024.fastq.gz | Fastqsanger.gz |
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Project description:To investigate ribosome localization and gene expression dynamics during starvation in cancer cells, we performed RNA sequencing and ribosome profiling in RKO cells under fed and starved (12.5 uM arginine) conditions.
2023-01-06 | GSE213472 | GEO
Project description:Background: Arginine deprivation was shown previously to inhibit retinoblastoma cell proliferation and induce cell death in vitro. However, the mechanisms by which retinoblastoma cells respond to arginine deprivation remain to be elucidated. Methods: Human derived retinoblastoma cell lines Y79 and WERI-Rb-1 were exposed to arginine depletion, and the effects on inhibiting cell growth and survival were evaluated. The study investigated potential mechanisms, including autophagy, cell cycle arrest, and apoptosis. Moreover, the roles of GCN2 and mTOR signaling pathways in these processes were examined. Results: We demonstrated that arginine deprivation effectively inhibited the growth of retinoblastoma cells in vitro. This treatment caused an increase in autophagic response. Additionally, we found that prolonged arginine shortage induced G2 cell cycle arrest and was accompanied by an increase in early apoptotic cells. Importantly, arginine depletion also caused an activation of GCN2 and an inhibition of mTOR signaling. We also discovered that the activation of SLC7A11 was regulated by GCN2 upon arginine deprivation. Knockdown of SLC7A11 rendered retinoblastoma cells partially resistant to arginine deprivation. Furthermore, we found that knockdown of GCN2 led to a decrease in autophagic response in WERI-Rb-1 cells and arrested more cells in S phase, which was accompanied by fewer apoptotic cells. Moreover, knockdown of GCN2 caused constant expression of ATF4, phosphorylation of 70S6K, and 4E-BP1 regardless of arginine deprivation. Conclusions: Collectively, our findings suggest that the GCN2-SLC7A11 axis regulates cell growth and survival upon arginine deprivation through coordinating autophagy, cell cycle arrest, and apoptosis in retinoblastoma cells. This work paves the way for the development of a novel treatment for retinoblastoma.
2024-10-28 | GSE278276 | GEO
Project description:Cancer cells heavily depend on the amino acid, glutamine, to meet the demands associated with growth and proliferation. Due to its rapid consumption, cancer cells frequently undergo glutamine starvation in vivo. We and others have shown that p53 is a critical regulator in metabolic stress resistance. To better understand the molecular mechanisms by which p53 activation promotes cancer cell adaptation to glutamine deprivation, we identified p53-dependent genes that are induced upon glutamine deprivation using RNA-seq analysis. We show that Slc7a3, an arginine transporter, is significantly induced by p53. We show the concomitant rise in intracellular arginine levels following glutamine deprivation is dependent on p53. The influx of arginine has minimal effect on known metabolic pathways upon glutamine deprivation. Instead, we found arginine serves as an effector for mTORC1 activation to promote in vitro and in vivo cell growth in response to glutamine starvation. Therefore, we identify a novel p53-inducible gene that contributes to the metabolic stress response.
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Project description:Purpose: To comprehensively identify the gene expression changes that occur after acute sleep deprivation. Method: We performed total RNA sequencing after 5hours of sleep deprivation. Results: Using total RNA-sequencing, we show that acute sleep deprivation causes dramatic gene expression changes in the mouse hippocampus. Conclusion: This study provides insight into the biological impact of acute sleep deprivation.
2021-03-01 | GSE166831 | GEO
Project description:Arginine is indispensable for both tumor progression and the function of immune cells, yet how arginine deprivation within the tumor microenvironment shapes anti-tumor immunity has remained unclear. In this study, we established an in vivo arginine-restriction model using a diet lacking arginine, which significantly suppressed tumor growth and activated global anti-tumor immune responses. Mechanistically, arginine deprivation triggered the integrated stress response in CD8+ T cells via the GCN2–cREL signaling axis, leading to elevated CD200 expression. These CD200+ CD8+ T cells in turn enhanced the antigen cross-presentation capacity of tumor-associated macrophages through CD200–CD200R interactions, forming a cooperative immune network that reinforced anti-tumor activity. Moreover, this arginine deprivation–induced cellular synergy improved the therapeutic efficacy of immunotherapy in colorectal cancer models. We further conducted a single-arm phase I clinical trial (NCT07038044), which demonstrated that an arginine-free diet is both feasible and safe for modulating systemic immunity in patients. Together, our findings provide a new conceptual framework for understanding the role of arginine in reshaping the tumor immune microenvironment and highlight arginine restriction as a promising and clinically translatable anti-tumor strategy.
2025-12-01 | GSE311149 | GEO
Project description:Arginine is indispensable for both tumor progression and the function of immune cells, yet how arginine deprivation within the tumor microenvironment shapes anti-tumor immunity has remained unclear. In this study, we established an in vivo arginine-restriction model using a diet lacking arginine, which significantly suppressed tumor growth and activated global anti-tumor immune responses. Mechanistically, arginine deprivation triggered the integrated stress response in CD8+ T cells via the GCN2–cREL signaling axis, leading to elevated CD200 expression. These CD200+ CD8+ T cells in turn enhanced the antigen cross-presentation capacity of tumor-associated macrophages through CD200–CD200R interactions, forming a cooperative immune network that reinforced anti-tumor activity. Moreover, this arginine deprivation–induced cellular synergy improved the therapeutic efficacy of immunotherapy in colorectal cancer models. We further conducted a single-arm phase I clinical trial (NCT07038044), which demonstrated that an arginine-free diet is both feasible and safe for modulating systemic immunity in patients. Together, our findings provide a new conceptual framework for understanding the role of arginine in reshaping the tumor immune microenvironment and highlight arginine restriction as a promising and clinically translatable anti-tumor strategy.
2025-12-01 | GSE311145 | GEO
Project description:Arginine is indispensable for both tumor progression and the function of immune cells, yet how arginine deprivation within the tumor microenvironment shapes anti-tumor immunity has remained unclear. In this study, we established an in vivo arginine-restriction model using a diet lacking arginine, which significantly suppressed tumor growth and activated global anti-tumor immune responses. Mechanistically, arginine deprivation triggered the integrated stress response in CD8+ T cells via the GCN2–cREL signaling axis, leading to elevated CD200 expression. These CD200+ CD8+ T cells in turn enhanced the antigen cross-presentation capacity of tumor-associated macrophages through CD200–CD200R interactions, forming a cooperative immune network that reinforced anti-tumor activity. Moreover, this arginine deprivation–induced cellular synergy improved the therapeutic efficacy of immunotherapy in colorectal cancer models. We further conducted a single-arm phase I clinical trial (NCT07038044), which demonstrated that an arginine-free diet is both feasible and safe for modulating systemic immunity in patients. Together, our findings provide a new conceptual framework for understanding the role of arginine in reshaping the tumor immune microenvironment and highlight arginine restriction as a promising and clinically translatable anti-tumor strategy.
2025-12-01 | GSE311146 | GEO
Project description:Arginine is indispensable for both tumor progression and the function of immune cells, yet how arginine deprivation within the tumor microenvironment shapes anti-tumor immunity has remained unclear. In this study, we established an in vivo arginine-restriction model using a diet lacking arginine, which significantly suppressed tumor growth and activated global anti-tumor immune responses. Mechanistically, arginine deprivation triggered the integrated stress response in CD8+ T cells via the GCN2–cREL signaling axis, leading to elevated CD200 expression. These CD200+ CD8+ T cells in turn enhanced the antigen cross-presentation capacity of tumor-associated macrophages through CD200–CD200R interactions, forming a cooperative immune network that reinforced anti-tumor activity. Moreover, this arginine deprivation–induced cellular synergy improved the therapeutic efficacy of immunotherapy in colorectal cancer models. We further conducted a single-arm phase I clinical trial (NCT07038044), which demonstrated that an arginine-free diet is both feasible and safe for modulating systemic immunity in patients. Together, our findings provide a new conceptual framework for understanding the role of arginine in reshaping the tumor immune microenvironment and highlight arginine restriction as a promising and clinically translatable anti-tumor strategy.
2025-12-01 | GSE311148 | GEO
Project description:Goals of the Study:; 1. Assess the scope of arginine-responsive hepatic gene expression using in vitro rat models. 2. Compare normal and tumorigenic cells; 3. Identify potentially novel genes and pathways that may be subject to amino acid (arginine) regulation; Background: We previously reported that mRNA levels of the tumor associated glycoprotein amino acid transporter TA1/LAT1/ CD98 light chain arginine increase in normal hepatic cells under low arginine conditions while levels are constitutive and high in hepatic tumor cells. This suggested LAT1 amino acid response was associated with the normal hepatic phenotype and lost in carcinogenesis and may impact cell growth and survival in the tumor microenvironment. We sought to investigate how many and what types of genes are responsive to a change in arginine levels over 18 hrs using an in vitro model system. Experimental design:; Differential gene expression was determined by microarrays using samples from triplicates of normal and transformed cells subjected to 18 hour arginine-deprivation compared to controls
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Project description:Altered hippocampal transcriptome dynamics following sleep deprivation
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