ArticleJournal of cancer research and clinical oncology2011
Efficacy of RNAi targeting of pyruvate kinase M2 combined with cisplatin in a lung cancer model.
Article in Journal of cancer research and clinical oncology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 96 citations in OpenAlex.
- Targeting Pyruvate Kinase M2: Signal Transduction Pathways and Exploration of Cancer Therapeutic Strategies.The AAPS journal · 2026Review
- Targeted metabolism creates possibilities for lung cancer treatment in the precision tumor era.Respiratory research · 2026Review
- TRAF6 promotes chemoresistance to paclitaxel of triple negative breast cancer via regulating PKM2-mediated glycolysis.Cancer medicine · 2023Article
- Isoalantolactone Suppresses Glycolysis and Resensitizes Cisplatin-Based Chemotherapy in Cisplatin-Resistant Ovarian Cancer Cells.International journal of molecular sciences · 2023Article
- Modulating Glycolysis to Improve Cancer Therapy.International journal of molecular sciences · 2023Review
- Structure-Guided Approach to Discover Tuberosin as a Potent Activator of Pyruvate Kinase M2, Targeting Cancer Therapy.International journal of molecular sciences · 2022Article
- Tumor metabolic reprogramming in lung cancer progression.Oncology letters · 2022Review
- Kaempferol Can Reverse the 5-Fu Resistance of Colorectal Cancer Cells by Inhibiting PKM2-Mediated Glycolysis.International journal of molecular sciences · 2022Article
- FBP1 regulates proliferation, metastasis, and chemoresistance by participating in C-MYC/STAT3 signaling axis in ovarian cancer.Oncogene · 2021Article
- Cisplatin Resistance and Redox-Metabolic Vulnerability: A Second Alteration.International journal of molecular sciences · 2021Review
- The Mechanism of Warburg Effect-Induced Chemoresistance in Cancer.Frontiers in oncology · 2021Review
- Inhibition of pyruvate dehydrogenase kinase‑1 by dicoumarol enhances the sensitivity of hepatocellular carcinoma cells to oxaliplatin via metabolic reprogramming.International journal of oncology · 2020Article
- TargetingInternational journal of molecular sciences · 2020Review
- Article
- Pyruvate Kinase M2 and Cancer: The Role of PKM2 in Promoting Tumorigenesis.Frontiers in oncology · 2020Review
- The role of pyruvate kinase M2 in anticancer therapeutic treatments.Oncology letters · 2019Review
- Review
- Acetylation accumulates PFKFB3 in cytoplasm to promote glycolysis and protects cells from cisplatin-induced apoptosis.Nature communications · 2018Article
- Metabolic rewiring in mutant Kras lung cancer.The FEBS journal · 2018Review
- Small ubiquitin-like modifier 1 modification of pyruvate kinase M2 promotes aerobic glycolysis and cell proliferation in A549 human lung cancer cells.OncoTargets and therapy · 2018Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposePyruvate kinase isoenzyme M2 (PKM2) is a key enzyme in aerobic glycolysis; inhibition of PKM2 leads to the tumor growth inhibition. In this study, the effects of combined treatment with cisplatin (DDP) and a plasmid that expresses a short hairpin RNA (shRNA) targeting PKM2 on the growth of human A549 xenograft lung cancer model were investigated.
methodsThe expression of PKM2 in A549 cells was determined by immunofluorescence. PKM2 expression levels were evaluated by Western blot analysis. In a human A549 lung cancer xenograft model, the effects of treatment with shRNA, with or without cisplatin, on tumor volume were determined. Apoptosis and cell proliferation status were examined to determine the mechanisms of tumor growth inhibition.
resultsExpression of shRNA targeting PKM2 resulted in inhibition of PKM2 expression in A549 cells. In the lung cancer xenograft model, average tumor volume in the group treated with both cisplatin and shRNA was statistically lower than those of other groups (P < 0.05). The levels of apoptotic cells were significantly higher in samples from animals in the combined treatment group than those from untreated animals (P < 0.05). The cell proliferation rate, as determined by counting cells labeled with an anti-phospho-histone H3, a marker for mitosis, was lower in samples from animals treated with both cisplatin and shRNA than in samples from other groups (P < 0.05).
conclusionsUse of RNA interfering (RNAi) targeting PKM2 significantly inhibited tumor growth when combined with cisplatin in a human A549 lung cancer xenograft model. The enhanced antitumor activity of the combined treatment compared to treatment with shRNA alone may result in part from increased induction of apoptosis and augmented inhibition of cancer cell proliferation.
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