ArticleOncogenesis2021
Diethyldithiocarbamate-copper complex (CuET) inhibits colorectal cancer progression via miR-16-5p and 15b-5p/ALDH1A3/PKM2 axis-mediated aerobic glycolysis pathway.
Article in Oncogenesis, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 73 citations in OpenAlex.
- The role of copper and cuproptosis in digestive system cancers: novel therapeutic strategies and mechanistic insights.Cancer biology & therapy · 2026Review
- Beyond Junk DNA: Emerging Roles of Non-Coding RNAs in Cancer and Therapeutic Innovation.Biomolecules · 2026Review
- Harnessing Cuproptosis for Antitumor Immunity: A Review of Current Evidence and Therapeutic Strategies.Molecular carcinogenesis · 2026Review
- Copper homeostasis and cuproptosis in cancer: mitochondrial metabolic dependency and nanomedicine-based therapeutic strategies.Apoptosis : an international journal on programmed cell death · 2026Review
- Glucose Metabolism Regulating Colorectal Cancer Initiation and Progression.Cancer science · 2026Review
- Tumor microenvironment-driven microRNA dysregulation: Key interactions in colorectal cancer progression.World journal of gastrointestinal oncology · 2026Review
- Cuproptosis: the mechanisms of copper-induced cell death and its implication in colorectal cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- The multifaceted role of microRNAs in colorectal cancer: pathogenesis and therapeutic implications.Non-coding RNA research · 2025Review
- In Silico Identification of circPIM1/miR-16-5p/miR-195-5p/PIM1 Feed-Forward Loop in Recurrent Grade 2 Meningioma.International journal of molecular sciences · 2025Article
- tsRNA-08614 inhibits glycolysis and histone lactylation by ALDH1A3 to confer oxaliplatin sensitivity in colorectal cancer.Translational oncology · 2025Article
- Essential and Non-Essential Metals and Metalloids and Their Role in Atherosclerosis.Cardiovascular toxicology · 2025Review
- SYT7 accelerates nasopharyngeal carcinoma progression via ALDH1A3-mediated STAT3 signaling activation.Oncogenesis · 2025Article
- Asymmetric cell division of ALDH1-positive cancer stem cells generates glycolytic metabolically diverse cell populations.Scientific reports · 2025Article
- Targeting PKM2 in cancer therapeutics: mechanistic advances and translational opportunities.Frontiers in immunology · 2025Review
- Unveiling the Cuproptosis in Colitis and Colitis-Related Carcinogenesis: A Multifaceted Player and Immune Moderator.Research (Washington, D.C.) · 2025Review
- β-lapachone suppresses carcinogenesis of cervical cancer via interaction with AKT1.Frontiers in pharmacology · 2025Article
- Construction of a novel copper-induced-cell-death-related gene signature for prognosis in colon cancer, with focus on KIF7.BMC cancer · 2024Article
- Deciphering the Role of Copper Homeostasis in Atherosclerosis: From Molecular Mechanisms to Therapeutic Targets.International journal of molecular sciences · 2024Review
- CuET overcomes regorafenib resistance by inhibiting epithelial-mesenchymal transition through suppression of the ERK pathway in hepatocellular carcinoma.Translational oncology · 2024Article
- Mechanisms of cuproptosis and its relevance to distinct diseases.Apoptosis : an international journal on programmed cell death · 2024Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Exploring novel anticancer drugs to optimize the efficacy may provide a benefit for the treatment of colorectal cancer (CRC). Disulfiram (DSF), as an antialcoholism drug, is metabolized into diethyldithiocarbamate-copper complex (CuET) in vivo, which has been reported to exert the anticancer effects on various tumors in preclinical studies. However, little is known about whether CuET plays an anti-cancer role in CRC. In this study, we found that CuET had a marked effect on suppressing CRC progression both in vitro and in vivo by reducing glucose metabolism. Mechanistically, using RNA-seq analysis, we identified ALDH1A3 as a target gene of CuET, which promoted cell viability and the capacity of clonal formation and inhibited apoptosis in CRC cells. MicroRNA (miR)-16-5p and 15b-5p were shown to synergistically regulate ALDH1A3, which was negatively correlated with both of them and inversely correlated with the survival of CRC patients. Notably, using co-immunoprecipitation followed with mass spectrometry assays, we identified PKM2 as a direct downstream effector of ALDH1A3 that stabilized PKM2 by reducing ubiquitination. Taken together, we disclose that CuET treatment plays an active role in inhibiting CRC progression via miR-16-5p and 15b-5p/ALDH1A3/PKM2 axis-mediated aerobic glycolysis pathway.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.