ArticleBritish journal of cancer2010
Dichloroacetate induces apoptosis and cell-cycle arrest in colorectal cancer cells.
Article in British journal of cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.
What it found
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The trial behind it
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Who cites it
90 citing papers in PubMed, 172 citations in OpenAlex.
- Case report: Sodium dichloroacetate (DCA) inhibition of the "Warburg Effect" in a human cancer patient: complete response in non-Hodgkin's lymphoma after disease progression with rituximab-CHOP.Journal of bioenergetics and biomembranes · 2013Trial
- Metal thiosemicarbazonates as dual mR2 RNR and colchicine-site tubulin inhibitors: from biochemical inhibition to mitotic arrest in MCF-7 breast cancer cells.Inorganic chemistry frontiers · 2026Article
- Beyond a Metabolite: Lactylation as a Pivotal Regulator of Colorectal Cancer Pathogenesis and Treatment Resistance.Journal of biochemical and molecular toxicology · 2026Review
- Chemical constituents in the rhizome of Curcuma longa and the pharmacological importance of curcumin hybrids.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026Review
- Hypoxic microenvironment in cancer: role in metabolic reprogramming.Frontiers in oncology · 2026Review
- Restricting metabolic plasticity enhances stress adaptation through the modulation of PDH and HIF1A in TRAP1-depleted colon cancer.Cancer letters · 2025Article
- "Non-Classical" Platinum Complexes: A Concise Review.International journal of molecular sciences · 2025Review
- Recent Advances on the Role of B Vitamins in Cancer Prevention and Progression.International journal of molecular sciences · 2025Review
- Impact of lactate on immune cell function in the tumor microenvironment: mechanisms and therapeutic perspectives.Frontiers in immunology · 2025Review
- Drug Repurposing: A Conduit to Unravelling Metabolic Reprogramming for Cancer Treatment.Mini reviews in medicinal chemistry · 2025Review
- Article
- Curcumin-Dichloroacetate Hybrid Molecule as an Antitumor Oral Drug against Multidrug-Resistant Advanced Bladder Cancers.Cancers · 2024Article
- Dichloroacetate for Cancer Treatment: Some Facts and Many Doubts.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Targeting Glucose Metabolism in Cancer Cells as an Approach to Overcoming Drug Resistance.Pharmaceutics · 2023Review
- Metabolic reprogramming induced by DCA enhances cisplatin sensitivity through increasing mitochondrial oxidative stress in cholangiocarcinoma.Frontiers in pharmacology · 2023Article
- Metformin is a metabolic modulator and radiosensitiser in rectal cancer.Frontiers in oncology · 2023Article
- Chemistry towards Biology-Instruct: Snapshot.International journal of molecular sciences · 2022Review
- Warburg effect in colorectal cancer: the emerging roles in tumor microenvironment and therapeutic implications.Journal of hematology & oncology · 2022Review
- Impact of Sodium Dichloroacetate Alone and in Combination Therapies on Lung Tumor Growth and Metastasis.International journal of molecular sciences · 2021Article
- Suppression of Pyruvate Dehydrogenase Kinase by Dichloroacetate in Cancer and Skeletal Muscle Cells Is Isoform Specific and Partially Independent of HIF-1α.International journal of molecular sciences · 2021Article
30 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCancer cells are highly dependent on glycolysis. Our aim was to determine if switching metabolism from glycolysis towards mitochondrial respiration would reduce growth preferentially in colorectal cancer cells over normal cells, and to examine the underlying mechanisms.
methodsRepresentative colorectal cancer and non-cancerous cell lines were treated with dichloroacetate (DCA), an inhibitor of pyruvate dehydrogenase kinase.
resultsDichloroacetate (20 mM) did not reduce growth of non-cancerous cells but caused significant decrease in cancer cell proliferation (P=0.009), which was associated with apoptosis and G(2) phase cell-cycle arrest. The largest apoptotic effect was evident in metastatic LoVo cells, in which DCA induced up to a ten-fold increase in apoptotic cell counts after 48 h. The most striking G(2) arrest was evident in well-differentiated HT29 cells, in which DCA caused an eight-fold increase in cells in G(2) phase after 48 h. Dichloroacetate reduced lactate levels in growth media and induced dephosphorylation of E1alpha subunit of pyruvate dehydrogenase complex in all cell lines, but the intrinsic mitochondrial membrane potential was reduced in only cancer cells (P=0.04).
conclusionsPyruvate dehydrogenase kinase inhibition attenuates glycolysis and facilitates mitochondrial oxidative phosphorylation, leading to reduced growth of colorectal cancer cells but not of non-cancerous cells.
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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.