ArticleProceedings of the National Academy of Sciences of the United States of America2009
Dicer-regulated microRNAs 222 and 339 promote resistance of cancer cells to cytotoxic T-lymphocytes by down-regulation of ICAM-1.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.
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Who cites it
104 citing papers in PubMed, 175 citations in OpenAlex.
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- Granulocyte colony-stimulating factor produces long-term changes in gene and microRNA expression profiles in CD34+ cells from healthy donors.Haematologica · 2014Trial
- MicroRNAs involvement in fludarabine refractory chronic lymphocytic leukemia.Molecular cancer · 2010Trial
- MicroRNA-targeted reprogramming of CD8+ T cells against cancer.Frontiers in immunology · 2026Review
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- Exosome-mediated Crosstalk in the Tumor Immune Microenvironment: Critical Drivers of Hepatocellular Carcinoma Progression.Journal of clinical and translational hepatology · 2025Review
- Mutations in glioblastoma proteins do not disrupt epitope presentation and recognition, maintaining a specific CD8 T cell immune response potential.Scientific reports · 2024Article
- CAR-mediated targeting of NK cells overcomes tumor immune escape caused by ICAM-1 downregulation.Journal for immunotherapy of cancer · 2024Article
- Acute myeloid leukemia-derived exosomes deliver miR-24-3p to hinder the T-cell immune response through DENN/MADD targeting in the NF-κB signaling pathways.Cell communication and signaling : CCS · 2023Article
- The dysregulation of miRNAs in epilepsy and their regulatory role in inflammation and apoptosis.Functional & integrative genomics · 2023Review
- Therapeutic and Diagnostic Potential of Exosomes as Drug Delivery Systems in Brain Cancer.Pharmaceutics · 2023Review
- MicroRNAs affecting the susceptibility of melanoma cells to CD8Clinical and translational medicine · 2023Article
- Role of exosomes in the development of the immune microenvironment in hepatocellular carcinoma.Frontiers in immunology · 2023Review
- Bone marrow CD3European journal of haematology · 2022Article
- MicroRNAs and drug resistance in colorectal cancer with special focus on 5-fluorouracil.Molecular biology reports · 2022Review
- Potential Therapeutic Effects of Melatonin Mediate via miRNAs in Cancer.Biochemical genetics · 2022Review
- Roles of intercellular cell adhesion molecule-1 (ICAM-1) in colorectal cancer: expression, functions, prognosis, tumorigenesis, polymorphisms and therapeutic implications.Frontiers in oncology · 2022Review
- OncomiRs as noncoding RNAs having functions in cancer: Their role in immune suppression and clinical implications.Frontiers in immunology · 2022Review
- A Darwinian perspective on tumor immune evasion.Biochimica et biophysica acta. Reviews on cancer · 2022Review
- The mutational repertoire of uterine sarcomas and carcinosarcomas in a Brazilian cohort: A preliminary study.Clinics (Sao Paulo, Brazil) · 2021Article
44 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
The RNase III endonuclease Dicer plays a key role in generation of microRNAs (miRs). We hypothesized that Dicer regulates cancer cell susceptibility to immune surveillance through miR processing. Indeed, Dicer disruption up-regulated intercellular cell adhesion molecule (ICAM)-1 and enhanced the susceptibility of tumor cells to antigen-specific lysis by cytotoxic T-lymphocytes (CTLs), while expression of other immunoregulatory proteins examined was not affected. Blockade of ICAM-1 inhibited the specific lysis of CTLs against Dicer-disrupted cells, indicating a pivotal role of ICAM-1 in the interaction between tumor cells and CTL. Both miR-222 and -339 are down-regulated in Dicer-disrupted cells and directly interacted with the 3' untranslated region (UTR) of ICAM-1 mRNA. Modulation of Dicer or these miRs inversely correlated with ICAM-1 protein expression and susceptibility of U87 glioma cells to CTL-mediated cytolysis while ICAM-1 mRNA levels remained stable. Immunohistochemical and in situ hybridization analyses of 30 primary glioblastoma tissues demonstrated that expression of Dicer, miR-222, or miR-339 was inversely associated with ICAM-1 expression. Taken together, Dicer is responsible for the generation of the mature miR-222 and -339, which suppress ICAM-1 expression on tumor cells, thereby down-regulating the susceptibility of tumor cells to CTL-mediated cytolysis. This study suggests development of novel miR-targeted therapy to promote cytolysis of tumor cells.
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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.