ArticleOncology letters2015
MicroRNA-181a enhances the chemotherapeutic sensitivity of chronic myeloid leukemia to imatinib.
Article in Oncology letters, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- Impact of non-coding RNAs on resistance to imatinib in chronic myelogenous leukemia.Leukemia research reports · 2025Review
- Role of miRNAs to control the progression of Chronic Myeloid Leukemia by their expression levels.Medical oncology (Northwood, London, England) · 2024Review
- miR-181a plays the tumor-suppressor role in chronic myeloid leukemia CD34Cellular and molecular life sciences : CMLS · 2023Article
- Article
- Antileukemic Activity of hsa-miR-203a-5p by Limiting Glutathione Metabolism in Imatinib-Resistant K562 Cells.Current issues in molecular biology · 2022Article
- Expression and role of nuclear receptor-interacting protein 1 (NRIP1) in stomach adenocarcinoma.Annals of translational medicine · 2020Article
- The Pervasive Role of the miR-181 Family in Development, Neurodegeneration, and Cancer.International journal of molecular sciences · 2020Review
- The expression and role of miR-181a in multiple myeloma.Medicine · 2018Article
- Overexpression of microRNA-15 increases the chemosensitivity of colon cancer cells to 5-fluorouracil and oxaliplatin by inhibiting the nuclear factor-κB signalling pathway and inducing apoptosis.Experimental and therapeutic medicine · 2018Article
- AQP8 inhibits colorectal cancer growth and metastasis by down-regulating PI3K/AKT signaling and PCDH7 expression.American journal of cancer research · 2018Article
- High expression of CPNE3 predicts adverse prognosis in acute myeloid leukemia.Cancer science · 2017Article
- Long-Term Exposure to Imatinib Mesylate Downregulates Hippo Pathway and Activates YAP in a Model of Chronic Myelogenous Leukemia.Stem cells and development · 2017Article
- Effects and Mechanism of Imatinib in Inhibiting Colon Cancer Cell Proliferation.Medical science monitor : international medical journal of experimental and clinical research · 2016Article
- Antitumor Activities of Green Tea by Up-regulation of miR-181a Expression in LNCaP Cells Using 3D Cell Culture Model.Avicenna journal of medical biotechnologyArticle
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNA-181 (miR-181) has been recently demonstrated to participate in the differentiation and development of immune cells, including natural killer cells and B and T lymphocytes, and myeloid linages, including erythroid and megakaryocytic cells. The aberrant expression of miR-181, particularly low expression levels, has been observed in a number of leukemia types, including B-cell chronic lymphocytic leukemia and cytogenetically abnormal acute myeloid leukemia. However, the expression and function of miR-181 in chronic myeloid leukemia (CML) remains unknown. In the present study, the aberrant expression of miR-181a was analyzed in a patient with CML and in the CML K562 cell line. In addition, the function and potential mechanisms of miR-181a in K562 cells with regard to their chemotherapeutic sensitivity to imatinib were investigated. The expression levels of miR-181a were significantly reduced in the patient with CML and in the CML K562 cell line. Furthermore, the overexpression of miR-181a in the K562 cells enhanced the chemotherapeutic sensitivity of these cells to imatinib. The potential mechanism mediating these effects may be associated with the capacity of miR-181a to inhibit cell growth and/or to induce cells apoptosis and differentiation in K562 cells. The results of the present study suggested that miR-181a may be a target for the treatment of CML and a useful indicator of the therapeutic sensitivity of CML to imatinib.
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