ArticleThe Journal of biological chemistry2012
Targeting of several glycolytic enzymes using RNA interference reveals aldolase affects cancer cell proliferation through a non-glycolytic mechanism.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 94 citations in OpenAlex.
- Functional dissection ofProceedings of the National Academy of Sciences of the United States of America · 2026Article
- O-GlcNAc and phosphorylation modifications on HtL1/FBA10 regulate wheat vernalization for flowering.Nature communications · 2025Article
- Catabolic rewiring in cancer impacts dietary interventions.Communications biology · 2025Review
- Aldolase A accelerates hepatocarcinogenesis by refactoring c-Jun transcription.Journal of pharmaceutical analysis · 2025Article
- Aldolase A: the broker of glycolysis.Nature metabolism · 2025Article
- Targeting aldolase A in hepatocellular carcinoma leads to imbalanced glycolysis and energy stress due to uncontrolled FBP accumulation.Nature metabolism · 2025Article
- Alcohol Alters Skeletal Muscle Bioenergetic Function: A Scoping Review.International journal of molecular sciences · 2024Article
- Beyond Glycolysis: Aldolase A Is a Novel Effector in Reelin-Mediated Dendritic Development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Oncogenic Alterations of Metabolism Associated with Resistance to Chemotherapy.Current molecular medicine · 2024Review
- Article
- ALDOC- and ENO2- driven glucose metabolism sustains 3D tumor spheroids growth regardless of nutrient environmental conditions: a multi-omics analysis.Journal of experimental & clinical cancer research : CR · 2023Article
- Moonlight functions of glycolytic enzymes in cancer.Frontiers in molecular biosciences · 2023Review
- Article
- Revisited Metabolic Control and Reprogramming Cancers by Means of the Warburg Effect in Tumor Cells.International journal of molecular sciences · 2022Review
- Incomptine A Induces Apoptosis, ROS Production and a Differential Protein Expression on Non-Hodgkin's Lymphoma Cells.International journal of molecular sciences · 2021Article
- ALDOA inhibits cell cycle arrest induced by DNA damage via the ATM-PLK1 pathway in pancreatic cancer cells.Cancer cell international · 2021Article
- Smoking shifts human small airway epithelium club cells toward a lesser differentiated population.NPJ genomic medicine · 2021Article
- Expression of Genes in the 16p11.2 Locus during Development of the Human Fetal Cerebral Cortex.Cerebral cortex (New York, N.Y. : 1991) · 2021Article
- Taurine Upregulates miRNA-122-5p Expression and Suppresses the Metabolizing Enzymes of Glycolytic Pathway in Hepatocellular Carcinoma.Molecular biology reports · 2021Article
- Proteomics analysis of protein biomarkers inJournal of traditional and complementary medicine · 2021Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In cancer, glucose uptake and glycolysis are increased regardless of the oxygen concentration in the cell, a phenomenon known as the Warburg effect. Several (but not all) glycolytic enzymes have been investigated as potential therapeutic targets for cancer treatment using RNAi. Here, four previously untargeted glycolytic enzymes, aldolase A, glyceraldehyde 3-phosphate dehydrogenase, triose phosphate isomerase, and enolase 1, are targeted using RNAi in Ras-transformed NIH-3T3 cells. Of these enzymes, knockdown of aldolase causes the greatest effect, inhibiting cell proliferation by 90%. This defect is rescued by expression of exogenous aldolase. However, aldolase knockdown does not affect glycolytic flux or intracellular ATP concentration, indicating a non-metabolic cause for the cell proliferation defect. Furthermore, this defect could be rescued with an enzymatically dead aldolase variant that retains the known F-actin binding ability of aldolase. One possible model for how aldolase knockdown may inhibit transformed cell proliferation is through its disruption of actin-cytoskeleton dynamics in cell division. Consistent with this hypothesis, aldolase knockdown cells show increased multinucleation. These results are compared with other studies targeting glycolytic enzymes with RNAi in the context of cancer cell proliferation and suggest that aldolase may be a useful target in the treatment of cancer.
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