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Developing a Prognostic Stratification Model Based on Glutathione Metabolism in Thyroid Cancer and Validating RRM2’s Tumor‑Promoting Role

ABSTRACT: Developing a Prognostic Stratification Model Based on Glutathione Metabolism in Thyroid Cancer and Validating RRM2’s Tumor‑Promoting Role

PROVIDER: PRJNA1291166 | ENA |

REPOSITORIES: ENA

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Developing a Prognostic Stratification Model Based on Glutathione Metabolism in Thyroid Cancer and Validating RRM2’s Tumor‑Promoting Role

Project description:Glutathione (GSH), the most abundant antioxidant in cells, acts as free radical scavenger and detoxifying agent. Elevation of GSH metabolism protects tumor from damage of oxidant and even promotes tumor progression. However, the clinical value of GSH metabolism in thyroid cancer (THCA) remained largely unknown. Collecting large THCA cohort from The Cancer Genome Atlas (TCGA) database, we systematically analyzed molecular characteristics of 24 GSH metabolism-related enzymes. GSH metabolism related enzymes including RRM2 and IDH2 were upregulated in tumor samples and negatively correlated with disease free survival (DFS). To expand the application of the GSH metabolism related enzymes in prognostic prediction, we for the first time built a risk stratification model based on the GSH metabolism related enzymes via LASSO Cox regression algorithm and validated its prediction performance. Patients were categorized into high- and low-risk groups according to the median of risk score. As supposed, high-risk patients suffered from dismal DFS. The key molecule in this process, RRM2, was screened by correlation analysis,and it was experimentally confirmed that the abnormally high expression of RRM2, which acts as a pro-carcinogenic molecule, enhances the proliferation, invasion, and migration of THCA cells in vitro and in vivo.

2025-07-19 | GSE302548 | GEO

Developing a prognostic stratification model based on glutathione metabolism in thyroid cancer and validating RRM2's tumor-promoting role.

Project description: Not available

| S-EPMC12665606 | biostudies-literature

Deng Lab RRM2 Acetylation Study

Project description:RRM2 Acetylation Mass Spectrometry Data including PD result files, raw mass spectrometry data and curated results.

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RNA sequencing of RRM2 overexpressing in LNCaP cells

Project description:Human prostate cancer LNCaP cells stably overexpress RRM2. Overexpression of RRM2 were confirm by westernblot or qPCR. Transfected cells were prepared for RNA-seq.

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CasID on RRM2 promoter region in neuroblastoma

Project description:dCas9-guided recruitment of the proximity ligation enzyme BirA* to the promoter region of RRM2 in SKNBE2c neuroblastoma cells.

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RNA sequencing of RRM2 overexpressing in PC-3 cells

Project description:Human prostate cancer PC-3 cells stably overexpress RRM2. Overexpression of RRM2 were confirm by westernblot or qPCR. Transfected cells were prepared for RNA-seq.

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RRM2 Promotes Liver Metastasis of Pancreatic Cancer by Stabilizing YBX1 and Activating the TGF-beta Pathway

Project description:Ribonucleotide reductase subunit M2 (RRM2) has been associated with various types of cancers and is related to tumor progression. However, the role of RRM2 in the liver metastasis of pancreatic cancer remains unclear. In this study, RRM2 was found to promote the malignant biological behavior of pancreatic cancer and enhance its liver metastasis. Further investigation into the downstream molecular mechanisms of RRM2 revealed that RRM2 stabilizes YBX1, upregulates TGFBR1, and activates the TGF-beta pathway to promote the progression and liver metastasis of pancreatic cancer. To further validate our hypothesis, we performed RNA sequencing under the specified conditions to determine the impact of RRM2 on downstream genes that can affect the liver metastasis of pancreatic cancer.

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Chimeric RNA RRM2-C2orf48 plays an oncogenic role in the development of NNK-induced lung cancer

Project description:Chimeric RNAs have been used as biomarkers and therapeutic targets for multiple types of cancers. However, less attention has been paid to their mechanism of action in neoplasia. Here, we report that chimeric RNA RRM2-C2orf48 promotes 4-(methyl nitrosamine)-1-(3-pyridinyl)-1-butanone (NNK)-induced lung cancer. We found that RRM2-C2orf48 had higher expression levels in lung cancer cell lines and in lung cancer tissues from 74 patients than in normal cells and tissues, respectively. And its expression level was correlated with smoking. Next, we demonstrate that the expression level of RRM2-C2orf48 could increase after treatment with 200 mg/L NNK for 24 h. Overexpressing RRM2-C2orf48 accelerated the process of NNK-induced lung cancer and promoted cell growth. Meanwhile, suppressing RRM2-C2orf48 inhibited cell growth. Finally, we identified miR-219a-2-3p as a potential target of RRM2-C2orf48. In summary, RRM2-C2orf48 accelerated the process of NNK-induced lung cancer and miR-219a-2-3p may be involved in this process.

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Metabolic gene expression-based stratification and prognostic risk predictive model validation studies

Project description:Metabolic gene expression-based stratification and prognostic risk predictive model of head and neck squamous cell carcinoma.

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RRM2-targeted nanocarrier enhances radiofrequency ablation efficacy in hepatocellular carcinoma through ferroptosis amplification and immune remodeling

Project description:Hepatocellular carcinoma (HCC) is associated with high mortality rates despite the widespread application of radiofrequency ablation (RFA), which has limited therapeutic efficacy as a monotherapy. This study investigated ribonucleotide reductase M2 (RRM2) upregulation in post-RFA HCC tissues and developed a targeted nanoco-delivery system (red blood cell membrane/cRGD-modified pH-sensitive liposomes [sS@RBCM/cRGD-phLips]) to increase RFA efficacy through specific RRM2 knockout. RRM2 knockout synergistically amplified RFA-induced tumor cell death by promoting ferroptosis and immunogenic cell death. Mechanistically, RRM2 knockout upregulated the STAT1–IRF1–acyl-CoA synthetase long-chain family member 4 axis, which potentiated lipid peroxidation and ferroptosis. Furthermore, the nanocarrier system enhanced dendritic cell maturation and cytotoxic T cell infiltration, thereby remodeling the tumor immune microenvironment. In vivo experiments revealed that the combination of RFA- and RRM2-targeted nanoparticles significantly suppressed tumor growth and prolonged survival in HCC-bearing mice with minimal systemic toxicity. Notably, the dual-loaded nanoparticles also enhanced the efficacy of anti-programmed cell death protein 1 therapy, suggesting a promising combinatorial approach for HCC treatment. This study presents a novel therapeutic strategy that integrates RRM2-targeted gene editing with RFA, offering a robust and synergistic approach for improving HCC outcomes.

2025-06-25 | GSE300290 | GEO

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