Copper homeostasis and cuproptosis in health and disease

Chen, Liyun; Min, Junxia; Wang, Fudi

doi:10.1038/s41392-022-01229-y

Cited by 457 publications

(338 citation statements)

References 284 publications

(379 reference statements)

Supporting

Mentioning

337

Contrasting

Order By: Relevance

“…Interestingly, FNBP4 coexpressed genes were involved in TCA cycle-related pathways including carbon metabolism, metabolism of xenobiotics by cytochrome P450, and oxidative phosphorylation. As the TCA cycle is closely related to cuproptosis, 32 FNBP4 may influence HCC progression through cuproptosis. Therefore, we explored the relationship between FNBP4 and cuproptosis regulators.…”

Section: Resultsmentioning

confidence: 99%

FNBP4 is a Potential Biomarker Associated with Cuproptosis and Promotes Tumor Progression in Hepatocellular Carcinoma

Zheng¹,

Zhang²,

Wu³

et al. 2023

IJGM

View full text Add to dashboard Cite

Background Hepatocellular carcinoma (HCC) is one of the most common malignant tumors that lacks an efficient therapeutic approach because of its elusive molecular mechanisms. This study aimed to investigate the biological function and potential mechanism of formin-binding protein 4 (FNBP4) in HCC. Methods FNBP4 expression in tissues and cells were detected by quantitative real-time PCR (qRT‒PCR), Western blot, and immunohistochemistry (IHC). The Kaplan-Meier method was used to explore the correlation between the FNBP4 expression and clinical survival. MTT, EdU incorporation, colony formation, and Transwell assays were performed to evaluate the function of FNBP4 in cell proliferation and migration in vitro. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis was used to explore the potential mechanism of FNBP4. The prognostic risk signature and nomogram were constructed to demonstrate the prognostic value of FNBP4. Results We found that FNBP4 was upregulated in patients with HCC and associated with poor overall survival (OS). Furthermore, knockdown of FNBP4 inhibited the proliferation and migration in HCC cells. Then, we performed a KEGG pathway analysis of the coexpressed genes associated with FNBP4 and found that FNBP4 may be associated with tumor-related signaling pathways and cuproptosis. We verified that FNBP4 could cause cell cycle progression and inactivation of the hippo signaling pathway. A prognostic risk signature containing three FNBP4-related differentially expressed cuproptosis regulators (DECRs) was established and can be used as an independent risk factor to evaluate the prognosis of patients with HCC. In addition, a nomogram including a risk score and clinicopathological factors was used to predict patient survival probabilities. Conclusion FNBP4, as a potential biomarker associated with cuproptosis, promotes HCC cell proliferation and metastasis. We provide a new potential strategy for HCC treatment by targeting FNBP4.

show abstract

Section: Resultsmentioning

confidence: 99%

FNBP4 is a Potential Biomarker Associated with Cuproptosis and Promotes Tumor Progression in Hepatocellular Carcinoma

Zheng¹,

Zhang²,

Wu³

et al. 2023

IJGM

View full text Add to dashboard Cite

show abstract

“…Knowledge of the mechanism of cuproptosis may help in designing a more effective anti-cancer nanomaterial. 15,55 Secondly, cuproptosis is a process closely related to cellular copper metabolism, so it is very important to reasonably control intracellular copper ion concentration in bothin vitro and in vivo studies. Regarding cancer, cuproptosis is a double-edged sword because it can not only kill cancer cells, but also induce copper toxicosis to destroy normal cells.…”

Section: Discussionmentioning

confidence: 99%

Cell death mediated by nanotechnology via the cuproptosis pathway: a novel horizon for cancer therapy

Wei

2023

Preprint

View full text Add to dashboard Cite

Cuproptosis, the current form of regulated cell death characterized by copper overload, oligomerization of lipoacylated proteins, and loss of the Fe-S cluster proteins, has been proposed to function closely with human diseases including cancer. Since the first identification in 2022, a wide range of strategies have been developed to induce cuproptosis for cancer therapy, such as small-molecule drugs and nanomaterials. Although many reviews related to cuproptosis have been reported, they remain at a basic mechanism level and a summary covering recent progress in the field of nanotechnologies in cuproptosis-based cancer therapy has not yet been presented. Therefore, it is time to fill the gap and shed light on future directions for the application of this promising tool to fight against cancer. In this minireview, we first expounded the mechanism of action of cuproptosis and emphasized the feasibility of triggering cuproptosis for cancer therapy. The recent progress of cancer treatments based on nanoparticle-induced cuproptosis was then described. Finally, the challenges and future development directions of the emerging field of cuproptosis were also discussed.

show abstract

“…Intracellular copper homeostasis is critical for cellular physiology and survival ( 24 ). Copper functions as a catalytic cofactor and drives many physiological processes, such as mitochondrial respiration, antioxidant defense, and bio-compound synthesis ( 25 ).…”

Section: Discussionmentioning

confidence: 99%

Development and validation of cuproptosis-related genes in synovitis during osteoarthritis progress

Chang

Hu²,

Chen³

et al. 2023

Front. Immunol.

View full text Add to dashboard Cite

Osteoarthritis (OA) is one of the most common refractory degenerative joint diseases worldwide. Synovitis is believed to drive joint cartilage destruction during OA pathogenesis. Cuproptosis is a novel form of copper-induced cell death. However, few studies have examined the correlations between cuproptosis-related genes (CRGs), immune infiltration, and synovitis. Therefore, we analyzed CRGs in synovitis during OA. Microarray datasets (GSE55235, GSE55457, GSE12021, GSE82107 and GSE176308) were downloaded from the Gene Expression Omnibus database. Next, we conducted differential and subtype analyses of CRGs across synovitis. Immune infiltration and correlation analyses were performed to explore the association between CRGs and immune cell abundance in synovitis. Finally, single-cell RNA-seq profiling was performed using the GSE176308 dataset to investigate the expression of CRGs in the various cell clusters. We found that the expression of five CRGs (FDX1, LIPT1, PDHA1, PDHB, and CDKN2A) was significantly increased in the OA synovium. Moreover, abundant and various types of immune cells infiltrated the synovium during OA, which was correlated with the expression of CRGs. Additionally, single-cell RNA-seq profiling revealed that the cellular composition of the synovium was complex and that their proportions varied greatly as OA progressed. The expression of CRGs differed across various cell types in the OA synovium. The current study predicted that cuproptosis may be involved in the pathogenesis of synovitis. The five screened CRGs (FDX1, LIPT1, PDHA1, PDHB, and CDKN2A) could be explored as candidate biomarkers or therapeutic targets for OA synovitis.

show abstract

Copper homeostasis and cuproptosis in health and disease

Cited by 457 publications

References 284 publications

FNBP4 is a Potential Biomarker Associated with Cuproptosis and Promotes Tumor Progression in Hepatocellular Carcinoma

FNBP4 is a Potential Biomarker Associated with Cuproptosis and Promotes Tumor Progression in Hepatocellular Carcinoma

Cell death mediated by nanotechnology via the cuproptosis pathway: a novel horizon for cancer therapy

Development and validation of cuproptosis-related genes in synovitis during osteoarthritis progress

Contact Info

Product

Resources

About