ArticleJournal of cellular and molecular medicine2016
Imiquimod-induced apoptosis of melanoma cells is mediated by ER stress-dependent Noxa induction and enhanced by NF-κB inhibition.
Article in Journal of cellular and molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 33 citations in OpenAlex.
- Detection of Circulating Tumour DNA in Plasma during the Treatment of In-transit Melanoma Metastases with Topical Imiquimod.Acta dermato-venereologica · 2026Article
- Redox processes in the treatment of advanced skin cancers.Clinical & experimental metastasis · 2026Review
- Immunomodulator loaded microneedle arrays for targeted intradermal drug delivery to skin tumors.Drug delivery · 2025Article
- TLR7/8 ligands R848 and imiquimod induce differentiation of bone marrow cells from patients with myelodysplastic syndrome towards mature neutrophils.Scientific reports · 2025Article
- Current Insights into the Role of UV Radiation-Induced Oxidative Stress in Melanoma Pathogenesis.International journal of molecular sciences · 2024Review
- Endoplasmic reticulum stress-a key guardian in cancer.Cell death discovery · 2024Review
- Anti-melanoma Effects of Resiquimod (RSQ) In Vitro and in Combination with Immune Checkpoint Blockade In Vivo.The AAPS journal · 2023Article
- The role of mitochondria in the resistance of melanoma to PD-1 inhibitors.Journal of translational medicine · 2023Review
- Crosstalk between endoplasmic reticulum stress and multidrug-resistant cancers: hope or frustration.Frontiers in pharmacology · 2023Review
- The Role of Calcium Signaling in Melanoma.International journal of molecular sciences · 2022Review
- The role of MAPK11/12/13/14 (p38 MAPK) protein in dopamine agonist-resistant prolactinomas.BMC endocrine disorders · 2021Article
- Article
- The Road of Solid Tumor Survival: From Drug-Induced Endoplasmic Reticulum Stress to Drug Resistance.Frontiers in molecular biosciences · 2021Review
- Melanoma stem cell maintenance and chemo-resistance are mediated by CD133 signal to PI3K-dependent pathways.Oncogene · 2020Article
- TLR4-mediated pyroptosis in human hepatoma-derived HuH-7 cells induced by a branched-chain polyunsaturated fatty acid, geranylgeranoic acid.Bioscience reports · 2020Article
- Transmissible Cancers and Immune Downregulation in Tasmanian Devil (Comparative medicine · 2019Article
- MEF2B is a member of the BCL6 gene transcriptional complex and induces its expression in diffuse large B-cell lymphoma of the germinal center B-cell-like type.Laboratory investigation; a journal of technical methods and pathology · 2019Article
- EAPB0503: An Imiquimod analog with potent in vitro activity against cutaneous leishmaniasis caused by Leishmania major and Leishmania tropica.PLoS neglected tropical diseases · 2018Article
- Transcriptome and proteome profiling reveals stress-induced expression signatures of imiquimod-treated Tasmanian devil facial tumor disease (DFTD) cells.Oncotarget · 2018Article
- Imiquimod inhibits growth and induces differentiation of myeloid leukemia cell lines.Cancer cell international · 2018Article
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Melanoma is characterized by dysregulated intracellular signalling pathways including an impairment of the cell death machinery, ultimately resulting in melanoma resistance, survival and progression. This explains the tumour's extraordinary resistance to the standard treatment. Imiquimod is a topical immune response modifier (imidazoquinoline) with both antiviral and antitumour activities. The mechanism by which imiquimod triggers the apoptosis of melanoma cells has now been carefully elucidated. Imiquimod-induced apoptosis is associated with the activation of apoptosis signalling regulating kinase1/c-Jun-N-terminal kinase/p38 pathways and the induction of endoplasmic stress characterized by the activation of the protein kinase RNA-like endoplasmic reticulum kinase signalling pathway, increase in intracellular Ca(2+) release, degradation of calpain and subsequent cleavage of caspase-4. Moreover, imiquimod triggers the activation of NF-κB and the expression of the inhibitor of apoptosis proteins (IAPs) such as, X-linked IAP (XIAP) together with the accumulation of reactive oxygen species (ROS). Also, imiquimod triggers mitochondrial dysregulation characterized by the loss of mitochondrial membrane potential (Δψm), the increase in cytochrome c release, and cleavage of caspase-9, caspase-3 and poly(ADP-ribose) polymerase (PARP). Inhibitors of specific pathways, permit the elucidation of possible mechanisms of imiquimod-induced apoptosis. They demonstrate that inhibition of NF-kB by the inhibitor of nuclear factor kappa-B kinase (IKK) inhibitor Bay 11-782 or knockdown of XIAP induces melanoma apoptosis in cells exposed to imiquimod. These findings support the use of either IKK inhibitors or IAP antagonists as adjuvant therapies to improve the effectiveness topical imiquimod in the treatment of melanoma.
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Registered trials
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.