Copper in cancer: friend or foe? - REVIEW - Metabolism, dysregulation, and therapeutic opportunities

Sep 23, 2026

Uploaded by Kyle

Review of copper’s dual role in cancer, framing copper as both a potential ally and a harmful factor. Discusses copper metabolism and its dysregulation as key drivers that can reshape cellular pathways linked to growth, survival, and death. Summarizes mechanistic connections between copper transport, chaperones, redox balance, mitochondrial function, and cancer progression. Highlights therapeutic opportunities that target copper handling to improve anticancer strategies.

LanguageEnglish

CategoryHealthcare

FormatPDF

Pages31

Reading Time1 h 18 min

AccessFree to download

Copper in cancer: friend or foe?

Metabolism, dysregulation, and therapeutic opportunities

DOI: 10.1002/cac2.70005 REVIEW Copper in cancer: friend or foe? Metabolism, dysregulation, and therapeutic opportunities Dan Shan1,2, 3 Peng Luo6 Shutong Liu1 Jinling Song4 Yuqing Ren5 Yuyuan Zhang1 Yuhao Ba1 Quan Cheng7 Hui Xu1 Siyuan Weng1 Anning Zuo1 Xinwei Han1, 8, 9 Jinhai Deng10 Zaoqu Liu1, 8, 9, 11 1 Department of Interventional Radiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, P. R. China 2University Hospital Galway, National University of Ireland Galway, Galway, Ireland 3 Department of Biobehavioral Sciences, Columbia University, New York, USA 4 Division of Pulmonology, Department of Pediatrics, The Third Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, P. R. China 5 Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, P. R. China 6The Department of Oncology, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong, P. R. China 7 Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, Hunan, P. R. China 8 Interventional Institute of Zhengzhou University, Zhengzhou, Henan, P. R. China 9 Interventional Treatment and Clinical Research Center of Henan Province, Zhengzhou, Henan, P. R. China 10 Richard Dimbleby Department of Cancer Research, Comprehensive Cancer Centre, Kings College London, London, UK 11 Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, P. R. China List of abbreviations: AD, Alzheimer’s disease; AIFM1/AIF, apoptosis inducing factor mitochondria associated 1/apoptosis inducing factor; ALDH, aldehyde dehydrogenase; AMPK, AMP-activated protein kinase; ATK, apoptosis tyrosine kinase; Atox1, antioxidant 1 copper chaperone; BCL, B-cell lymphoma; BRCA, breast cancer; Cco, cytochrome C oxidase; CCS, cytochrome c oxidase copper chaperone; CDKN2A, cyclin-dependent kinase inhibitor 2A; CDT, chemodynamic therapy; CNV, copy number variation; COMMD10, copper metabolism MURR1 domain 10; COX, cytochrome C oxidase; COX17, cytochrome C oxidase17; CP, ceruloplasmin; CRC, colorectal cancer; CRIP2, copper response element-binding protein 2; CSCs, cancer stem cells; CTR1, copper transporter 1; Cu3BiS3, Cu-and Bi-based bimetal chalcogenide; Cu-Cy, cupro-cysteamine; CuET, copper-containing metabolites; DBH, dopamine beta-hydroxylase; DBT, dihydrolipoamide branched chain transacylase; DDR, DNA damage response; DDTC, diethyl dithiocarbamate; DLAT, dihydrolipoamide acetyltransferase; DLST, dihydrolipoamide S-acetyltransferase; DMT1, divalent metal transporter 1; DSF, disulfiram; ERK, extracellular signal-regulated kinase; ERK, extracellular signal-regulated protein kinase; ES, elesclomol; FABP3, fatty acid binding protein 3; FABP7, fatty acid binding protein 7; FDX1, ferredoxin 1; FGF, fibroblast growth factor; GCSH, glycine cleavage system H protein; GPX, cystathione peroxidase; GPX4, glutathione peroxidase 4; GSH, glutathione; GST, glutathione-S-transferase; HCC, hepatocellular carcinoma; HD, Huntington’s disease; HIF1, hypoxia-inducible factor 1; HIF1α, hypoxia-inducible factor 1 subunit α; HMGB1, high-mobility group box 1; HNSCC, head and neck squamous cell carcinoma; HTT, huntingtin; HZIFCu, Cu2+-doped hollow zeolite imidazoline framework nanoparticles; IGF, insulin-like growth factor; IL-1α, inflammatory cytokine; IL-1β, interleukin-1 beta; IMS, mitochondrial membrane space; KIRC, kidney renal clear cell carcinoma; LA, lipoic acid; LDH, lactate dehydrogenase; LIHC, liver hepatocellular carcinoma; LUAD, lung adenocarcinoma; MAP2K1, mitogen-activated proteinkinase kinase 1; MAPK, mitogen-activated protein kinase; MBDs, metal-binding domains; MEK, mitogen-activated proteinkinase kinase; MEK1, mitogen-activated protein kinase 1; MICOS, mitochondrial contact site and cristae organizing system; MLKL, mixed lineage kinase domain-like; MOF, metal-organic framework;

FAQs

What is the central question of the review?

How copper functions in cancer—whether it acts more as a friend or a foe—and what metabolic mechanisms underlie that duality.

Which biological processes does the review focus on?

Copper metabolism and dysregulation, emphasizing pathway-level effects related to cancer cell regulation and dysfunction.

How does the review connect copper biology to therapy?

By identifying therapeutic opportunities that exploit abnormal copper handling in tumors to support anticancer intervention strategies.

Sep 23, 2026

Uploaded by Kyle