ArticlePharmaceuticals (Basel, Switzerland)2022
Indole-3-Carbinol Stabilizes p53 to Induce miR-34a, Which Targets LDHA to Block Aerobic Glycolysis in Liver Cancer Cells.
Article in Pharmaceuticals (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Alkaloids mediated regulation of microRNA in cancer: molecular insights and emerging therapeutic strategies.Frontiers in oncology · 2026Review
- EMSY enhances glycolysis in ovarian cancer cells.European journal of medical research · 2025Article
- Review
- Indole-3-carbinol prevented tumor progression and potentiated PD1ab therapy by upregulating PTEN in colorectal cancer.Discover oncology · 2025Article
- Hydroxysafflor Yellow A Mitigates Sepsis-Induced Pulmonary and Intestinal Injury by Inhibiting TP53 Mediated Ferroptosis.Infection and drug resistance · 2025Article
- Follicular fluid-derived extracellular vesicles miR-34a-5p regulates granulosa cell glycolysis in polycystic ovary syndrome by targeting LDHA.Journal of ovarian research · 2024Article
- UBE2C enhances temozolomide resistance by regulating the expression of p53 to induce aerobic glycolysis in glioma.Acta biochimica et biophysica Sinica · 2024Article
- Withaferin A Inhibits Liver Cancer Tumorigenesis by Suppressing Aerobic Glycolysis through the p53/IDH1/HIF-1α Signaling Axis.Current cancer drug targets · 2024Article
- The Southern European Atlantic Diet and Its Supplements: The Chemical Bases of Its Anticancer Properties.Nutrients · 2023Review
- Review
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Certain cancer cells prefer aerobic glycolysis rather than oxidative phosphorylation for energy supply. Lactate dehydrogenase A (LDHA) catalyzes the reduction of pyruvate to lactate and regains NAD+ so that glycolysis is continued. As a pivotal enzyme to promote smooth glycolysis, LDHA plays an important role in carcinogenesis. Indole-3-carbinol (I3C) has displayed antitumor activity, but the exact mechanism remains to be identified. In this study, we treated liver cancer cells with I3C, performed colony formation and cell migration, measured the expression of glycolysis-related proteins, and predicted and validated LDHA-targeting miRNA from the databases. In addition, the mRNA and protein levels of p53, glycolysis-related genes and miRNAs that regulate glycolysis were detected after I3C and siRNA-p53 treatment alone or in combination. Next, the expression and colocalization of p53 and MDM2 in liver cancer cells were evaluated after I3C treatment, and the effect of I3C on p53 protein stability was examined. The results showed that I3C inhibited cell proliferation, migration, and the expression levels of glycolysis-related gene LDHAs. MiR-34a was predicted to target LDHA, and I3C downregulated its expression. Furthermore, the combined I3C and siRNA-p53 treatment demonstrated that I3C regulated the expression of LDHA via miR-34a in a p53-dependent manner. Finally, I3C inhibited MDM2 expression and its colocalization with p53 and stabilized p53 expression. In summary, I3C inhibited the degradation of p53 by MDM2 in liver cancer cells; stable p53 induced miR-34a, which targeted LDHA, a key enzyme for aerobic glycolysis, suggesting cancer metabolism is an important target for I3C in liver cancer cells.
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