PDE3B regulates KRT6B and increases the sensitivity of bladder cancer cells to copper ionophores

Feng, Yuankang; Huang, Zhenlin; Song, Liang; Li, Ningyang; Li, Xiang; Shi, Huihui; Liu, Ruoyang; Lu, Fubo; Han, Xu; Ding, Yafei; Ding, Yinghui; Wang, Jun; Yang, Jinjian; Jia, Zhankui

doi:10.1007/s00210-023-02928-1

Cited by 4 publications

References 47 publications

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Copper homeostasis and copper-induced cell death in tumor immunity: implications for therapeutic strategies in cancer immunotherapy

Zhang,

Huang,

et al. 2024

Biomark Res

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Copper is an important trace element for maintaining key biological functions such as cellular respiration, nerve conduction, and antioxidant defense. Maintaining copper homeostasis is critical for human health, and its imbalance has been linked to various diseases, especially cancer. Cuproptosis, a novel mechanism of copper-induced cell death, provides new therapeutic opportunities for metal ion regulation to interact with cell fate. This review provides insights into the complex mechanisms of copper metabolism, the molecular basis of cuproptosis, and its association with cancer development. We assess the role of cuproptosis-related genes (CRGs) associated with tumorigenesis, their importance as prognostic indicators and therapeutic targets, and the impact of copper homeostasis on the tumor microenvironment (TME) and immune response. Ultimately, this review highlights the complex interplay between copper, cuproptosis, and cancer immunotherapy.

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Copper homeostasis and copper-induced cell death in tumor immunity: implications for therapeutic strategies in cancer immunotherapy

Zhang,

Huang,

et al. 2024

Biomark Res

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Bulk RNA analysis identified the characteristics and immunoinvasive patterns of osimertinib resistance in patients with non-small cell lung cancer

Shi,

Qiu,

Shi

et al. 2024

Preprint

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Non-small cell lung cancer (NSCLC) remains a leading cause of cancer-related mortality worldwide, with epidermal growth factor receptor (EGFR) mutations being a common driver. Osimertinib, a third-generation EGFR tyrosine kinase inhibitor (TKI), has shown efficacy in treating NSCLC patients harboring EGFR mutations. However, resistance to osimertinib poses a significant clinical challenge. This study aims to identify key genes associated with osimertinib resistance in NSCLC and elucidate their underlying mechanisms to inform new therapeutic strategies. Utilizing a comprehensive bioinformatics approach, we conducted differential expression analysis, enrichment analysis, consensus clustering, drug sensitivity analysis, protein-protein interaction (PPI) network construction, and immune infiltration analysis. Our findings revealed 126 genes, including KRT14, KRT16, KRT17, KRT5, KRT6A, KRT6B, TP63, and TRIM29, that are potentially pivotal in osimertinib resistance. Enrichment analyses indicated significant involvement in biological processes such as epidermis development and keratinocyte differentiation, and pathways like valine, leucine, and isoleucine degradation. Immune infiltration analysis showed significant downregulation of 14 immune cell types in the resistant group, with notable negative correlations between hub genes and specific immune cells. We constructed a diagnostic model with an area under the curve (AUC) greater than 0.9,,validated externally, demonstrating robust diagnostic performance. Interaction networks, including mRNA-TF, RBP-mRNA, and lncRNA-miRNA-mRNA, provided insights into the complex regulatory mechanisms of resistance.

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Novel insights into cuproptosis inducers and inhibitors

Zhang,

Deng,

Liu

et al. 2024

Front. Mol. Biosci.

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Cuproptosis is a new pattern of Cu-dependent cell death distinct from classic cell death pathways and characterized by aberrant lipoylated protein aggregation in TCA cycle, Fe-S cluster protein loss, HSP70 elevation, proteotoxic and oxidative stress aggravation. Previous studies on Cu homeostasis and Cu-induced cell death provide a great basis for the discovery of cuproptosis. It has gradually gathered enormous research interests and large progress has been achieved in revealing the metabolic pathways and key targets of cuproptosis, due to its role in mediating some genetic, neurodegenerative, cardiovascular and tumoral diseases. In terms of the key targets in cuproptosis metabolic pathways, they can be categorized into three types: oxidative stress, mitochondrial respiration, ubiquitin-proteasome system. And strategies for developing cuproptosis inducers and inhibitors involved in these targets have been continuously improved. Briefly, based on the essential cuproptosis targets and metabolic pathways, this paper classifies some relevant inducers and inhibitors including small molecule compounds, transcription factors and ncRNAs with the overview of principle, scientific and medical application, in order to provide reference for the cuproptosis study and target therapy in the future.

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PDE3B regulates KRT6B and increases the sensitivity of bladder cancer cells to copper ionophores

Cited by 4 publications

References 47 publications

Copper homeostasis and copper-induced cell death in tumor immunity: implications for therapeutic strategies in cancer immunotherapy

Copper homeostasis and copper-induced cell death in tumor immunity: implications for therapeutic strategies in cancer immunotherapy

Bulk RNA analysis identified the characteristics and immunoinvasive patterns of osimertinib resistance in patients with non-small cell lung cancer

Novel insights into cuproptosis inducers and inhibitors

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