RNA-seq for orthotopic lung tumor treated with taurine and proline
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1188604 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31416684_1.fastq.gz | Fastqsanger.gz | |||
| SRR31416684_2.fastq.gz | Fastqsanger.gz | |||
| SRR31416685_1.fastq.gz | Fastqsanger.gz | |||
| SRR31416685_2.fastq.gz | Fastqsanger.gz | |||
| SRR31416686_1.fastq.gz | Fastqsanger.gz |
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Project description:This study aimed to clarify their role in lung cancer progression, offering insights into potential therapeutic targets. This is the first study to reveal the promoting effects of taurine and proline in lung cancer, suggesting a link to poorer prognosis.
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Project description:Background: Metabolic dysregulation has been implicated in bronchopulmonary dysplasia development. Taurine is an essential amino acid for neonates and is critically involved in glucose and fatty acid metabolism. Neonatal tissue obtains taurine mainly through the taurine transporter. The biological role of taurine in neonatal lung development has never been explored. As glucose metabolism mechanistically modulates angiogenesis and angiogenesis is the central player for neonatal lung development, we hypothesize that taurine depletion contributes to bronchopulmonary dysplasia development. Results: Although most genes and proteins for oxidative phosphorylation were enriched in hyperoxia pup lungs, the complex-1 activity decreased. The decrease in taurine-dependent complex-1 core subunits, ND5 and ND6, in hyperoxia lungs reasonably explained the discrepancy. Metabolomics analysis demonstrated decreased lung taurine with increased blood taurine of hyperoxia pups, compatible with the decreased taurine transporter expression. Decreased glycosylation and increased degradation explained the decreased taurine transporter expression. The results of the complementary study using tunicamycin and tauroursodeoxycholic acid studies supported that endoplasmic reticulum stress contributes to decreased taurine transporter expression in hyperoxia lungs. The effect of taurine treatment on reducing endoplasmic reticulum stress, increasing ND5 and ND6 expression, angiogenesis, and, most importantly, the alveolar formation is beneficial to hyperoxia rat pups. Conclusion: Hyperoxia exposure causes endoplasmic reticulum stress, increases taurine transporter degradation, and leads to taurine depletion in the neonatal lungs with subsequent metabolic dysregulation, resulting in poor alveolar formation of the neonatal lungs. We provide evidence of the never-being-reported protective role of taurine in neonatal lung development. The fact that taurine attenuates the severity of bronchopulmonary dysplasia by reducing hyperoxia-induced endoplasmic reticulum stress and mitochondrial dysfunction indicates its therapeutic potential for treating bronchopulmonary dysplasia.
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Project description:An orthotopic lung xenograft model was used to identify differential expression of lung CTCs in comparison to primary lung tumor cells.
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Project description:Chronic lung diseases significantly impact the aging population globally, but their etiology is largely unknown, and the therapeutic options are minimal. Cellular senescence has been increasingly recognized as an essential driving mechanism for chronic lung diseases. Remodeling in subcellular compartments is commonly observed in senescent cells, which reciprocally regulates the senescent progression. Roles of peroxisomes in cellular senescence have been documented, but the molecular mechanisms for this regulation remain poorly understood. Here, we showed that the peroxisome pathway and the shuttling receptor PEX5 are downregulated during replicative and oxidative senescence in human fetal lung fibroblast 1 (HFL-1) cells. PEX5 knockdown can induce senescence via transcriptional suppression of LAMP1 and autophagic flux. Further study revealed that activation of the p38 MAPK signaling pathway and subsequent nuclear localization of transcription factor EB (TFEB) are the significant retrograde signals contributing to the PEX5 regulation of cellular senescence. Metabolomics analysis identified a substantial increase in taurine levels in cells with PEX5 overexpression. Reciprocally, treatment of cells with taurine enhanced PEX5 levels in the senescent HFL-1 cells and the lungs of aged mice and alleviated senescence, suggesting the presence of a taurine-dependent response in PEX5 regulation of cellular senescence. Collectively, our findings provided new insights into the peroxisomal regulation of cellular senescence by integrating the p38 MAPK retrograde signaling pathway and taurine metabolism, which may help develop anti-aging strategies to treat chronic lung diseases.
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Project description:Analysis of skeletal muscle from taurine transporter (TauT) knockout mice at 3 or 18 months of age. Knocking out TauT result in a decrease in muscle cell size, impaired exercise capacity and accelerated muscle aging. Results provide molecular insights into physiological role of taurine.
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Project description:An orthotopic model of lung cancer was established in Rag-2 null mice by injecting 1 x 106 GFP-A549 cells into the mouse lung via the trachea. After 6 weeks a primary tumor develops in the right lung. RNA was collected from tumors established in the orthotopic model after 6 weeks in three separate mice and from the right lung of three sham control mice that were injected with PBS by the same method. RNA was also collected from the A549 cells in culture. RNA was applied to an Affymetrix Customized Protease Microarray (HuMu ProtIn chip). This custom chip is able to distinguish human and mouse genes by using oligonucleotides specific for each species. The chip contains all known human and mouse proteases and protease inhibitors. A distribution of gene expression from a comparison of all human and mouse genes present in the tumor vs. the control lung was indentified as well as a distribution of gene expression from a comparison of all human and mouse genes present in the tumor vs. the cells in culture. Human and mouse genes differentially expressed in each group were identifed.
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Project description:Osteoradionecrosis of the jaw (ORNJ) is a severe complication following head and neck radiotherapy that significantly impacts the quality of life of patients. Currently, there is a lack of comprehensive understanding of the microenvironmental factors involved in ORNJ. In this study, we reveal the activation of taurine metabolism in irradiated mandibular stromal cells using scRNA-Seq and demonstrate a decrease in taurine levels in irradiated bone marrow mesenchymal stromal cells (BMSCs) through metabolomics. Compared with unirradiated BMSCs, taurine uptake in irradiated BMSCs increases. Taurine concentrations in the peripheral blood and jaws of irradiated mice are significantly lower than those in unirradiated mice (P = 0.0064 and 0.0249 respectively). Supplementation with taurine promotes osteogenic differentiation, reduces oxidative stress, and decreases DNA damage in irradiated BMSCs. Oral administration of taurine significantly improves the survival rate of irradiated mice and enhances osteogenesis in irradiated jaws. Our study highlights the role of taurine in the recovery from radiation-induced jaw injury, and suggests its potential as a non-invasive therapeutic option for combating ORNJ.
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Project description:Taurine-respiring gut bacteria produce H2S with ambivalent impact on host health. We report the isolation and ecophysiological characterization of the first taurine-respiring mouse gut bacterium. Taurinivorans muris represents a new widespread species that differs from the human gut sulfidogen Bilophila wadsworthia in its sulfur metabolism pathways and host distribution. T. muris specializes in taurine respiration in vivo, seemingly unaffected by mouse diet and genotype, but is dependent on other bacteria for release of taurine from bile acids. This dataset contains the total proteomic data from three independent growth conditions.
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