Selenocysteine tRNA methylation promotes oxidative stress resistance in melanoma metastasis
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ABSTRACT:
PROVIDER: PRJNA1129129 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29632400.fastq.gz | Fastqsanger.gz | |||
| SRR29632401.fastq.gz | Fastqsanger.gz | |||
| SRR29632402.fastq.gz | Fastqsanger.gz | |||
| SRR29632403.fastq.gz | Fastqsanger.gz | |||
| SRR29632404.fastq.gz | Fastqsanger.gz |
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Project description:Oxidative stress has been shown to limit metastasis of numerous cancer types including melanoma. A specialized group of 25 proteins containing the 21st amino acid, selenocysteine, plays a central role in oxidative stress resistance, which is a key driver of metastasis. A single selenocysteine tRNA methylation, Um34, is required for the translation of several stress-related selenoproteins in a selenium-dependent manner. Herein, we characterize FTSJ1 as the Um34 methyltransferase and show that its activity is required for the Sec tRNA (tRNASec) Um34 modification. Loss of Um34 affects translation of a subset of selenoproteins and increases melanoma cell sensitivity to oxidative stress while increased Um34 levels promote oxidative stress resistance. Loss of FTSJ1 does not affect primary melanoma tumor growth but abolishes metastatic spread in vivo. Overexpression of FTSJ1 specifically increases melanoma metastasis in vivo. Our work establishes FTSJ1 as the Um34 methyltransfearse and tRNASec Um34 modification as a central regulator of oxidative stress resistance during melanoma metastasis.
2024-09-03 | GSE270971 | GEO
Project description:Oxidative stress has been shown to limit metastasis of numerous cancer types including melanoma. A specialized group of 25 proteins containing the 21st amino acid, selenocysteine, plays a central role in oxidative stress resistance, which is a key driver of metastasis. A single selenocysteine tRNA methylation, Um34, is required for the translation of several stress-related selenoproteins in a selenium-dependent manner. Herein, we characterize FTSJ1 as the Um34 methyltransferase and show that its activity is required for the Sec tRNA (tRNASec) Um34 modification. Loss of Um34 affects translation of a subset of selenoproteins and increases melanoma cell sensitivity to oxidative stress while increased Um34 levels promote oxidative stress resistance. Loss of FTSJ1 does not affect primary melanoma tumor growth but abolishes metastatic spread in vivo. Overexpression of FTSJ1 specifically increases melanoma metastasis in vivo. Our work establishes FTSJ1 as the Um34 methyltransfearse and tRNASec Um34 modification as a central regulator of oxidative stress resistance during melanoma metastasis.
2024-09-03 | GSE270976 | GEO
Project description:selenocysteine tRNA methylation promotes oxidative stress resistance in melanoma metastasis [Xenograft Human]
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Project description:The relationship between loss of hypothalamic function and onset of diabetes mellitus remains elusive. Therefore, we generated a targeted oxidative-stress murine model utilizing conditional knockout of selenocysteine-tRNA (Trsp) using rat insulin promoter-driven-Cre (RIP-Cre). These Trsp-knockout (TrspRIPKO) mice exhibit deletion of Trsp in both hypothalamic cells and pancreatic β-cells leading to increased hypothalamic oxidative stress and severe insulin resistance. Leptin signals were suppressed and numbers of proopiomelanocortin-positive neurons in the hypothalamus were decreased. In contrast, a Trsp-knockout mouse (TrspIns1KO) expressing Cre specifically in pancreatic β-cells, but not in the hypothalamus, did not display insulin and leptin resistance, demonstrating a critical role of the hypothalamus in the onset of diabetes mellitus. Nrf2 (NF-E2-related-factor-2) regulates antioxidant gene expression. Gene-driven increase in Nrf2 signaling suppressed hypothalamic oxidative stress and improved insulin and leptin resistance in TrspRIPKO mice. Thus, Nrf2 harbors the potential to prevent the onset of diabetic mellitus by reducing hypothalamic oxidative damage.
2017-02-06 | GSE92235 | GEO
Project description:The relationship between loss of hypothalamic function and onset of diabetes mellitus remains elusive. Therefore, we generated a targeted oxidative-stress murine model utilizing conditional knockout of selenocysteine-tRNA (Trsp) using rat insulin promoter-driven-Cre (RIP-Cre). These Trsp-knockout (TrspRIPKO) mice exhibit deletion of Trsp in both hypothalamic cells and pancreatic β-cells leading to increased hypothalamic oxidative stress and severe insulin resistance. Leptin signals were suppressed and numbers of proopiomelanocortin-positive neurons in the hypothalamus were decreased. In contrast, a Trsp-knockout mouse (TrspIns1KO) expressing Cre specifically in pancreatic β-cells, but not in the hypothalamus, did not display insulin and leptin resistance, demonstrating a critical role of the hypothalamus in the onset of diabetes mellitus. Nrf2 (NF-E2-related-factor-2) regulates antioxidant gene expression. Gene-driven increase in Nrf2 signaling suppressed hypothalamic oxidative stress and improved insulin and leptin resistance in TrspRIPKO mice. Thus, Nrf2 harbors the potential to prevent the onset of diabetic mellitus by reducing hypothalamic oxidative damage.
2017-02-06 | GSE92234 | GEO
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Project description:This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/In this experiment, we have injected mice with fluorescent melanoma cells and then collected their lungs 1-3 days later and run them through a flow cytometer to separate the fluorescent cells (i.e., the melanoma cells) from the non-sluprescent cells (i.e., the lung cells) so we can sequence their transcriptomes to identify the transciptional profiles associated with pulmonary melanoma metastasis.
2014-08-20 | E-ERAD-287 | biostudies-arrayexpress
Project description:Metastasis is the deadliest phase of cancer progression. Experimental models using immunodeficient mice have been used to gain insights into the mechanisms of metastasis. We report here the identification of a “metastasis aggressiveness gene expression signature” derived using human melanoma cells selected based on their metastatic potentials in a xenotransplant metastasis model. Comparison with expression data from human melanoma patients shows that this metastasis gene signature correlates with the aggressiveness of melanoma metastases in human patients. Many genes encoding secreted and membrane proteins are included in the signature, suggesting the importance of tumor-microenvironment interactions during metastasis. Keywords: disease state
2007-10-02 | GSE8401 | GEO