Molecular typing and prognostic model of lung adenocarcinoma based on cuprotosis-related lncRNAs

Zheng, Miaosen; Zhou, Hao; Xie, Jing; Zhang, Haifeng; Shen, Xiaojian; Zhu, Dongbing

doi:10.21037/jtd-22-1534

Cited by 3 publications

(2 citation statements)

References 65 publications

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“…With the same technology in pancreatic ductal adenocarcinoma patients, Some LncRNA s are thought to have strong correlations with ductal adenocarcinoma outcomes, including AC005332.6, LINC02041, LINC00857, and AL117382 ( Chi et al, 2022 ). The same results in lung adenocarcinoma were seen ( Zheng M. et al, 2022 ). Cuprotosis can affect the polarization and function of tumor-associated macrophages (TAMs), which are immune cells that play a crucial role in the tumor microenvironment.…”

Section: Mechanism Of Targeting Copper or Cuprotosis In Cancer Treatmentsupporting

confidence: 79%

Targeting copper metabolism: a promising strategy for cancer treatment

Kong

Sun

2023

Front. Pharmacol.

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Copper is an essential micronutrient that plays a critical role in many physiological processes. However, excessive copper accumulation in cancer cells has been linked to tumor growth and metastasis. This review article explores the potential of targeting copper metabolism as a promising strategy for cancer treatment. Excessive copper accumulation in cancer cells has been associated with tumor growth and metastasis. By disrupting copper homeostasis in cancer cells and inducing cell death through copper-dependent mechanisms (cuproplasia and cuprotosis, respectively), therapies can be developed with improved efficacy and reduced side effects. The article discusses the role of copper in biological processes, such as angiogenesis, immune response, and redox homeostasis. Various approaches for targeting copper metabolism in cancer treatment are examined, including the use of copper-dependent enzymes, copper-based compounds, and cuprotosis-related genes or proteins. The review also explores strategies like copper chelation therapy and nanotechnology for targeted delivery of copper-targeting agents. By understanding the intricate network of cuprotosis and its interactions with the tumor microenvironment and immune system, new targets for therapy can be identified, leading to improved cancer treatment outcomes. Overall, this comprehensive review highlights the significant potential of targeting copper metabolism as a promising and effective approach in cancer treatment, while providing valuable insights into the current state of research in this field.

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Section: Mechanism Of Targeting Copper or Cuprotosis In Cancer Treatmentsupporting

confidence: 79%

Targeting copper metabolism: a promising strategy for cancer treatment

Kong

Sun

2023

Front. Pharmacol.

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“…As importantly functional molecules in HCC, lncRNAs have been intensively investigated. [47][48][49] Many HCC-related lncRNAs show aberrant expression and correlation with prognosis of HCC patients. [50][51][52] However, the contribution of m 6 A modification to the expression and role of lncRNAs are still largely unclear.…”

Section: Discussionmentioning

confidence: 99%

N6-Methyladenosine-Modified ATP8B1-AS1 Exerts Oncogenic Roles in Hepatocellular Carcinoma via Epigenetically Activating MYC

Tan,

Huang,

Huang

et al. 2023

JHC

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Purpose N 6 -methyladenosine (m 6 A) modification has shown critical roles in regulating mRNA fate. Non-coding RNAs also have important roles in various diseases, including hepatocellular carcinoma (HCC). However, the potential influences of m 6 A modification on non-coding RNAs are still unclear. In this study, we identified a novel m 6 A-modified ATP8B1-AS1 and aimed to investigate the effects of m 6 A on the expression and role of ATP8B1-AS1 in HCC. Methods qPCR was performed to measure the expression of related genes. The correlation between gene expression and prognosis was analyzed using public database. m 6 A modification level was measured using MeRIP and single-base elongation- and ligation-based qPCR amplification method. The roles of ATP8B1-AS1 in HCC were investigated using in vitro and in vivo functional assays. The mechanisms underlying the roles of ATP8B1-AS1 were investigated by ChIRP and ChIP assays. Results ATP8B1-AS1 is highly expressed in HCC tissues and cell lines. High expression of ATP8B1-AS1 is correlated with poor overall survival of HCC patients. ATP8B1-AS1 is m 6 A modified and the 792 site of ATP8B1-AS1 is identified as an m 6 A modification site. m 6 A modification increases the stability of ATP8B1-AS1 transcript. m 6 A modification level of ATP8B1-AS1 is increased in HCC tissues and cell lines, and correlated with poor overall survival of HCC patients. ATP8B1-AS1 promotes HCC cell proliferation, migration, and invasion, which were abolished by the mutation of m 6 A-modified 792 site. Mechanistic investigation revealed that m 6 A-modified ATP8B1-AS1 interacts with and recruits m 6 A reader YTHDC1 and histone demethylase KDM3B to MYC promoter region, leading to the reduction of H3K9me2 level at MYC promoter region and activation of MYC transcription. Functional rescue assays showed that depletion of MYC largely abolished the oncogenic roles of ATP8B1-AS1. Conclusion m 6 A modification level of ATP8B1-AS1 is increased and correlated with poor prognosis in HCC. m 6 A-modified ATP8B1-AS1 exerts oncogenic roles in HCC via epigenetically activating MYC expression.

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Copper homeostasis dysregulation in respiratory diseases: a review of current knowledge

Song,

Yue,

Zhang

et al. 2024

Front. Physiol.

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Cu is an essential micronutrient for various physiological processes in almost all human cell types. Given the critical role of Cu in a wide range of cellular processes, the local concentrations of Cu and the cellular distribution of Cu transporter proteins in the lung are essential for maintaining a steady-state internal environment. Dysfunctional Cu metabolism or regulatory pathways can lead to an imbalance in Cu homeostasis in the lungs, affecting both acute and chronic pathological processes. Recent studies have identified a new form of Cu-dependent cell death called cuproptosis, which has generated renewed interest in the role of Cu homeostasis in diseases. Cuproptosis differs from other known cell death pathways. This occurs through the direct binding of Cu ions to lipoylated components of the tricarboxylic acid cycle during mitochondrial respiration, leading to the aggregation of lipoylated proteins and the subsequent downregulation of Fe-S cluster proteins, which causes toxic stress to the proteins and ultimately leads to cell death. Here, we discuss the impact of dysregulated Cu homeostasis on the pathogenesis of various respiratory diseases, including asthma, chronic obstructive pulmonary disease, idiopathic interstitial fibrosis, and lung cancer. We also discuss the therapeutic potential of targeting Cu. This study highlights the intricate interplay between copper, cellular processes, and respiratory health. Copper, while essential, must be carefully regulated to maintain the delicate balance between necessity and toxicity in living organisms. This review highlights the need to further investigate the precise mechanisms of copper interactions with infections and immune inflammation in the context of respiratory diseases and explore the potential of therapeutic strategies for copper, cuproptosis, and other related effects.

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Molecular typing and prognostic model of lung adenocarcinoma based on cuprotosis-related lncRNAs

Cited by 3 publications

References 65 publications

Targeting copper metabolism: a promising strategy for cancer treatment

Targeting copper metabolism: a promising strategy for cancer treatment

N6-Methyladenosine-Modified ATP8B1-AS1 Exerts Oncogenic Roles in Hepatocellular Carcinoma via Epigenetically Activating MYC

Copper homeostasis dysregulation in respiratory diseases: a review of current knowledge

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