The implications and prospect of cuproptosis-related genes and copper transporters in cancer progression

Zhao, Qianwen; Qi, Tonggang

doi:10.3389/fonc.2023.1117164

Cited by 13 publications

(8 citation statements)

References 73 publications

(56 reference statements)

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“…Higher FDX1 expression is associated with better disease-free survival (DFS) and overall survival (OS) in renal cancer, liver hepatocellular carcinoma, LUAD, and lung squamous cell carcinoma [ 14 ]. Furthermore, FDX1 expression is linked to specific immune subtypes in ACC, BRCA, KIRP, KIRC, LIHC, LGG, PRAD (prostate adenocarcinoma), SARC, STAD, THCA, and UCEC (uterine corpus endometrial carcinoma) [ 7 , 15 ]. In this context, our study revealed a significant down-regulation of FDX1 in LUAD tissues compared to adjacent normal tissues.…”

Section: Discussionmentioning

confidence: 99%

“…Copper, an essential trace element, plays a pivotal role in various biological processes such as cellular respiration, antioxidant defense, and enzymatic reactions [ 17 ]. However, an imbalance in copper homeostasis can result in cytotoxicity, triggering cuproptosis [ 15 ]. In this process, elevated copper levels disrupt cellular redox balance, leading to oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

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Ferredoxin 1: a gatekeeper in halting lung adenocarcinoma progression through activation of the GPRIN2 signaling pathway

Liu,

Wu,

et al. 2024

J Transl Med

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Background Lung adenocarcinoma (LUAD) is a highly lethal form of lung cancer. Despite advancements in treatments, managing LUAD is still challenging due to its aggressive behavior. Recent studies indicate that various molecular pathways, including the dysregulation of ferredoxin 1 (FDX1), play roles in LUAD progression. FDX1, a crucial protein in cellular redox reactions and energy metabolism, has been linked to several cancers. However, its exact role in the development of LUAD is not yet fully understood. Methods We investigated the role of ferredoxin 1 (FDX1) in LUAD progression through analysis of its expression in LUAD tissues and its impact on patient survival. Functional assays were performed to assess the effects of FDX1 overexpression on LUAD cell proliferation, migration, and invasion. A xenograft model was employed to evaluate the tumorigenesis potential of LUAD cells with FDX1 overexpression. Mechanistic insights into FDX1 regulation were gained through depletion experiments targeting the G protein-regulated inducer of neurite outgrowth 2 (GPRIN2)/PI3K signaling pathway. Results FDX1 expression was down-regulated in LUAD tissues, correlating with shorter patient survival. Overexpression of FDX1 suppressed LUAD cell proliferation, migration, and invasion in vitro, and inhibited tumorigenesis in vivo. Mechanistically, the GPRIN2/PI3K signaling pathway was implicated in FDX1 regulation, as depletion of GPRIN2 reversed the effects of FDX1 overexpression on cellular functions. Conclusions Our findings highlight FDX1 as a potential tumor suppressor in LUAD, acting through modulation of the GPRIN2/PI3K signaling pathway. These results suggest FDX1 as a promising therapeutic target for LUAD treatment, warranting further investigation into its clinical relevance.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Ferredoxin 1: a gatekeeper in halting lung adenocarcinoma progression through activation of the GPRIN2 signaling pathway

Liu,

Wu,

et al. 2024

J Transl Med

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“…While the role of copper in breast cancer, particularly its impact on the immune microenvironment and immunotherapy, has been well-established ( 42 ), the association between seven key cuproptosis-associated genes and breast cancer remains unexplored. These genes include PGK1 (mitochondrial metabolism and tumorigenesis), SLC family members SLC52A2 and SLC16A6 (metabolic transport), SEC14L2 (vitamin E uptake), RAD23B (nucleotide excision repair and apoptosis), CCL5 (inflammatory cell migration) and MAL2 (transcytosis in hepatocellular carcinoma) ( 43 - 58 ).…”

Section: Cuproptosis and Breast Cancermentioning

confidence: 99%

Revolutionizing breast cancer treatment: Harnessing the related mechanisms and drugs for regulated cell death (Review)

Ai,

Yi,

Qiu

et al. 2024

Int J Oncol

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Breast cancer arises from the malignant transformation of mammary epithelial cells under the influence of various carcinogenic factors, leading to a gradual increase in its prevalence. This disease has become the leading cause of mortality among female malignancies, posing a significant threat to the health of women. The timely identification of breast cancer remains challenging, often resulting in diagnosis at the advanced stages of the disease. Conventional therapeutic approaches, such as surgical excision, chemotherapy and radiotherapy, exhibit limited efficacy in controlling the progression and metastasis of the disease. Regulated cell death (RCD), a process essential for physiological tissue cell renewal, occurs within the body independently of external influences. In the context of cancer, research on RCD primarily focuses on cuproptosis, ferroptosis and pyroptosis. Mounting evidence suggests a marked association between these specific forms of RCD, and the onset and progression of breast cancer. For example, a cuproptosis vector can effectively bind copper ions to induce cuproptosis in breast cancer cells, thereby hindering their proliferation. Additionally, the expression of ferroptosis-related genes can enhance the sensitivity of breast cancer cells to chemotherapy. Likewise, pyroptosis-related proteins not only participate in pyroptosis, but also regulate the tumor microenvironment, ultimately leading to the death of breast cancer cells. The present review discusses the unique regulatory mechanisms of cuproptosis, ferroptosis and pyroptosis in breast cancer, and the mechanisms through which they are affected by conventional cancer drugs. Furthermore, it provides a comprehensive overview of the significance of these forms of RCD in modulating the efficacy of chemotherapy and highlights their shared characteristics. This knowledge may provide novel avenues for both clinical interventions and fundamental research in the context of breast cancer.

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“…Copper uptake outside the cell is performed by copper transporter 1 (CTR1, encoded by SLC31A1), and the expression of CTR1 prevents excessive copper from entering the cell. Studies have proved that CTR1 is highly expressed in the liver tissues of liver cancer patients, and CTR1 mediates copper to indirectly affect the cell signaling cascade and promote tumorigenesis and development [ 15 , 16 ]. Jianping, G. et al revealed that copper ions activate protein kinase B (PKB, also known as AKT) through CTR1 and demonstrated that copper can bind phosphoinositol-dependent protein kinase 1 (PDK1) and enhance the interaction between PDK1 and AKT, thereby activating phosphoinositol kinase 3 (PI3K)-AKT Carcinogenic signaling pathways promote the occurrence of cancer [ 17 ].…”

Section: Copper Transporter and Iron Transporter In Liver Cancermentioning

confidence: 99%

Immunomodulation of cuproptosis and ferroptosis in liver cancer

Mo,

Zhang,

et al. 2024

Cancer Cell Int

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According to statistics, the incidence of liver cancer is increasing yearly, and effective treatment of liver cancer is imminent. For early liver cancer, resection surgery is currently the most effective treatment. However, resection does not treat the disease in advanced patients, so finding a method with a better prognosis is necessary. In recent years, ferroptosis and cuproptosis have been gradually defined, and related studies have proved that they show excellent results in the therapy of liver cancer. Cuproptosis is a new form of cell death, and the use of cuproptosis combined with ferroptosis to inhibit the production of hepatocellular carcinoma cells has good development prospects and is worthy of in-depth discussion by researchers. In this review, we summarize the research progress on cuproptosis combined with ferroptosis in treating liver cancer, analyze the value of cuproptosis and ferroptosis in the immune of liver cancer, and propose potential pathways in oncotherapy with the combination of cuproptosis and ferroptosis, which can provide background knowledge for subsequent related research.

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The implications and prospect of cuproptosis-related genes and copper transporters in cancer progression

Cited by 13 publications

References 73 publications

Ferredoxin 1: a gatekeeper in halting lung adenocarcinoma progression through activation of the GPRIN2 signaling pathway

Ferredoxin 1: a gatekeeper in halting lung adenocarcinoma progression through activation of the GPRIN2 signaling pathway

Revolutionizing breast cancer treatment: Harnessing the related mechanisms and drugs for regulated cell death (Review)

Immunomodulation of cuproptosis and ferroptosis in liver cancer

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