ArticleOncotarget2014
Targeting aerobic glycolysis and HIF-1alpha expression enhance imiquimod-induced apoptosis in cancer cells.
Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.
- Role of bone marrow adipocytes in bone metastasis development and progression: a systematic review.Frontiers in endocrinology · 2023Pooled it
- Regulation of Autophagy and Metabolism in Hepatocellular Carcinoma: Involvement of Wnt-β-Catenin Pathway.Journal of cellular and molecular medicine · 2026Article
- M1 macrophage membrane-engineered PLGA nanoparticles reprogram M2 tumor-associated macrophages to enhance anti-tumor immunity in breast cancer.Journal of materials science. Materials in medicine · 2026Article
- Article
- Modulating the tumor microenvironment in a mouse model of colon cancer using a combination of HIF-1α inhibitors and Toll-Like Receptor 7 agonists.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- The Protective Effects of Mcl-1 on Mitochondrial Damage and Oxidative Stress in Imiquimod-Induced Cancer Cell Death.Cancers · 2024Article
- Riluzole regulates pancreatic cancer cell metabolism by suppressing the Wnt-β-catenin pathway.Scientific reports · 2022Article
- Recent advances in cancer immunotherapy: Modulation of tumor microenvironment by Toll-like receptor ligands.BioImpacts : BI · 2022Review
- Molecular Chaperones: Molecular Assembly Line Brings Metabolism and Immunity in Shape.Metabolites · 2020Review
- Salmonella enterica serovar Typhimurium sseK3 induces apoptosis and enhances glycolysis in macrophages.BMC microbiology · 2020Article
- Inhibitors of HSP90 in melanoma.Apoptosis : an international journal on programmed cell death · 2020Review
- LCAL1 enhances lung cancer survival via inhibiting AMPK-related antitumor functions.Molecular and cellular biochemistry · 2019Article
- Metabolic profiling of cancer cells reveals genome-wide crosstalk between transcriptional regulators and metabolism.Nature communications · 2019Article
- cAMP Receptor Protein of Salmonella enterica Serovar Typhimurium Modulate Glycolysis in Macrophages to Induce Cell Apoptosis.Current microbiology · 2019Article
- Toll-like receptors in immunity and inflammatory diseases: Past, present, and future.International immunopharmacology · 2018Review
- Transcriptome and proteome profiling reveals stress-induced expression signatures of imiquimod-treated Tasmanian devil facial tumor disease (DFTD) cells.Oncotarget · 2018Article
- Article
- Bone marrow adipocytes promote the Warburg phenotype in metastatic prostate tumors via HIF-1α activation.Oncotarget · 2016Article
- Metabonomics applied in exploring the antitumour mechanism of physapubenolide on hepatocellular carcinoma cells by targeting glycolysis through the Akt-p53 pathway.Scientific reports · 2016Article
- Article
Corrections and comments
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Authors and funding
8 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor cells rely on aerobic glycolysis to maintain unconstrained cell growth and proliferation. Imiquimod (IMQ), a synthetic Toll-like receptor (TLR) 7/8 ligand, exerts anti-tumor effects directly by inducing cell death in cancer cells and/or indirectly by activating cellular immune responses against tumor cells. However, whether IMQ modulates glucose metabolism pathways remains unclear. In this study, we demonstrated that IMQ can enhance aerobic glycolysis by up-regulating HIF-1α expression at the transcriptional and translational levels via ROS mediated STAT3- and Akt-dependent pathways, independent of TLR7/8 signaling. The genetic silencing of HIF-1α not only repressed IMQ-induced aerobic glycolysis but also sensitized cells to IMQ-induced apoptosis due to faster ATP and Mcl-1 depletion. Moreover, the glucose analog 2-DG and the Hsp90 inhibitor 17-AAG, which destabilizes the HIF-1α protein, synergized with IMQ to induce tumor cell apoptosis in vitro and significantly inhibited tumor growth in vivo. Thus, we hypothesize that the IMQ-induced up-regulation of HIF-1α and aerobic glycolysis is a protective response to the metabolic stress generated by IMQ treatment, and thus, co-treatment with inhibitors of HIF-1α and/or glycolysis may be a useful therapeutic strategy to enhance the anti-tumor effects of IMQ in clinical settings.
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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.