MiR-30e induces apoptosis and sensitizes K562 cells to imatinib treatment via regulation of the BCR–ABL protein

التفاصيل البيبلوغرافية
العنوان: MiR-30e induces apoptosis and sensitizes K562 cells to imatinib treatment via regulation of the BCR–ABL protein
المؤلفون: Noam Shomron, Amos Toren, Metsada Pasmanik-Chor, Oshrat Hershkovitz-Rokah, Pia Raanani, Shira Modai, Galit Granot, Ofer Shpilberg
المصدر: Cancer Letters. 356:597-605
بيانات النشر: Elsevier BV, 2015.
سنة النشر: 2015
مصطلحات موضوعية: Cancer Research, Blotting, Western, Fusion Proteins, bcr-abl, Antineoplastic Agents, Apoptosis, Biology, Real-Time Polymerase Chain Reaction, Piperazines, Fusion gene, Leukemia, Myelogenous, Chronic, BCR-ABL Positive, hemic and lymphatic diseases, microRNA, Tumor Cells, Cultured, medicine, Humans, RNA, Messenger, neoplasms, Cell Proliferation, ABL, Reverse Transcriptase Polymerase Chain Reaction, Hematopoietic stem cell, Myeloid leukemia, Imatinib, Gene Expression Regulation, Neoplastic, MicroRNAs, Pyrimidines, medicine.anatomical_structure, Oncology, Drug Resistance, Neoplasm, Benzamides, Imatinib Mesylate, Cancer research, Tyrosine kinase, medicine.drug, K562 cells
الوصف: Chronic myeloid leukemia (CML) is a disorder of hematopoietic stem cell carrying the Philadelphia (Ph) chromosome and an oncogenic BCR-ABL fusion gene. Tyrosine kinase inhibitors (TKIs) of the BCR-ABL kinase are the treatment of choice for CML patients. Imatinib was the first TKI used in clinical practice with excellent results. MicroRNAs (miRNAs) are short non-coding regulatory RNAs that control gene expression and play an important role in cancer development and progression. Aberrant miRNA expression profiles have been shown to be characteristic of many cancers. Here, we demonstrate that miR-30e is expressed at low levels in CML cell lines and patient samples. Bioinformatics analysis reveals a putative target site for miR-30e in the 3'-untranslated region (UTR) of the ABL gene. In agreement, luciferase assay verified that miR-30e directly targets ABL. Enforced expression of miR-30e in K562 cells suppressed proliferation and induced apoptosis of these cells and sensitized them to imatinib treatment. These findings strongly suggest that miR-30e acts as a tumor suppressor by downregulating BCR-ABL expression. Up-regulation of miR-30e in CML cells may therefore have a therapeutic efficacy against this disease.
تدمد: 0304-3835
DOI: 10.1016/j.canlet.2014.10.006
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::9d9809c6c767cc371df6f457c1e34d0e
https://doi.org/10.1016/j.canlet.2014.10.006
Rights: CLOSED
رقم الانضمام: edsair.doi.dedup.....9d9809c6c767cc371df6f457c1e34d0e
قاعدة البيانات: OpenAIRE
الوصف
تدمد:03043835
DOI:10.1016/j.canlet.2014.10.006