ArticleCancer science2019
p53/Lactate dehydrogenase A axis negatively regulates aerobic glycolysis and tumor progression in breast cancer expressing wild-type p53.
Article in Cancer science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.
- Interplay Between Glucose Metabolism and Chromatin Modifications in Cancer.Frontiers in cell and developmental biology · 2021Pooled it
- Rethinking residual p53 function in HPV-positive cervical cancer cells.Journal of virology · 2026Article
- Targeting phase separation: a new strategy to disrupt the stromal-immune axis in colorectal cancer.Cell communication and signaling : CCS · 2026Review
- FBXO39 promotes LDHA-mediated aerobic glycolysis and colorectal cancer progression by p53 degradation.Journal of translational medicine · 2026Article
- Tackling cuproptosis: from metabolic rewiring to therapeutic exploitation in cancer.Cellular & molecular immunology · 2026Review
- Metabolic Vulnerabilities as a Therapeutic Target in Breast Cancer.Current oncology (Toronto, Ont.) · 2026Review
- The cross-talk and interplay between ferroptosis and cuproptosis in tumor and therapeutics.Cellular oncology (Dordrecht, Netherlands) · 2026Review
- The SOX12-YBX1-LDHA signaling axis drives metastasis in papillary thyroid carcinoma.Cell death & disease · 2025Article
- Molecular signatures of disulfidptosis: interplay with programmed cell death pathways and therapeutic implications in oncology.Cellular & molecular biology letters · 2025Review
- Article
- Metabolic regulation by p53: Implications for cancer therapy.Molecules and cells · 2025Review
- "Friends or foes": a new perspective of tumour metabolic transcriptional modification.Cell death & disease · 2025Review
- Diallyl Trisulfide Enhances Doxorubicin Chemosensitivity by Inhibiting the Warburg Effect and Inducing Apoptosis in Breast Cancer Cells.Journal of Cancer · 2025Article
- Development of human lactate dehydrogenase a inhibitors: high-throughput screening, molecular dynamics simulation and enzyme activity assay.Journal of computer-aided molecular design · 2024Article
- UBE2C enhances temozolomide resistance by regulating the expression of p53 to induce aerobic glycolysis in glioma.Acta biochimica et biophysica Sinica · 2024Article
- Metabolic Roles of HIF1, c-Myc, and p53 in Glioma Cells.Metabolites · 2024Review
- Targeting mitochondrial bioenergetics by combination treatment with imatinib and dichloroacetate in human erythroleukemic K‑562 and colorectal HCT‑116 cancer cells.International journal of oncology · 2024Article
- The genomic alterations in glioblastoma influence the levels of CSF metabolites.Acta neuropathologica communications · 2024Article
- Cuproptosis: p53-regulated metabolic cell death?Cell death and differentiation · 2023Review
- p53 Modulates Radiosensitivity in Head and Neck Cancers-From Classic to Future Horizons.Diagnostics (Basel, Switzerland) · 2022Review
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Authors and funding
15 authors at 2 institutions in 4 countries.
Funding
Abstract
Tumor suppressor p53 is a master regulator of apoptosis and plays key roles in cell cycle checkpoints. p53 responds to metabolic changes and alters metabolism through several mechanisms in cancer. Lactate dehydrogenase A (LDHA), a key enzyme in glycolysis, is highly expressed in a variety of tumors and catalyzes pyruvate to lactate. In the present study, we first analyzed the association and clinical significance of p53 and LDHA in breast cancer expressing wild-type p53 (wt-p53) and found that LDHA mRNA levels are negatively correlated with wt-p53 but not with mutation p53 mRNA levels, and low p53 and high LDHA expression are significantly associated with poor overall survival rates. Furthermore, p53 negatively regulates LDHA expression by directly binding its promoter region. Moreover, a series of LDHA gain-of-function and rescore experiments were carried out in breast cancer MCF7 cells expressing endogenous wt-p53, showing that ectopic expression of p53 decreases aerobic glycolysis, cell proliferation, migration, invasion and tumor formation of breast cancer cells and that restoration of the expression of LDHA in p53-overexpressing cells could abolish the suppressive effect of p53 on aerobic glycolysis and other malignant phenotypes. In conclusion, our findings showed that repression of LDHA induced by wt-p53 blocks tumor growth and invasion through downregulation of aerobic glycolysis in breast cancer, providing new insights into the mechanism by which p53 contributes to the development and progression of breast cancer.
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