title: Altered expression of miR-181a and miR-146a does not change the expression of surface NCRs in human NK cells.
abstract: MicroRNAs (miRNAs) play an important role in regulating gene expression and immune responses. Of interest, miR-181a and miR-146a are key players in regulating immune responses and are among the most abundant miRNAs expressed in NK cells. Bioinformatically, we predicted miR-181a to regulate the expression of the natural cytotoxicity receptor NCR2 by seeded interaction with the 3'-untranslated region (3'-UTR). Whereas, miR-146a expression was not significantly different (P = 0.7361), miR-181a expression was, on average 10-fold lower in NK cells from breast cancer patients compared to normal subjects; P < 0.0001. Surface expression of NCR2 was detected in NK cells from breast cancer patients (P = 0.0384). While cytokine receptor-induced NK cell activation triggered overexpression of miR-146a when stimulated with IL-2 (P = 0.0039), IL-15 (P = 0.0078), and IL-12/IL-18 (P = 0.0072), expression of miR-181a was not affected. Overexpression or knockdown of miR-181a or miR-146a in primary cultured human NK cells did not affect the level of expression of any of the three NCRs; NCR1, NCR2 or NCR3 or NK cell cytotoxicity. Expression of miR-181a and miR-146a did not correlate to the expression of the NCRs in NK cells from breast cancer patients or cytokine-stimulated NK cells from healthy subjects.
authors.affiliation: Microbiology and Immunology Department, German University in Cairo (GUC), New Cairo, Egypt.
authors.forename: Mona
authors.initials: M
authors.lastname: Rady
authors.affiliation: Immunology Department, Leibniz Research Center for Working Environment and Human Factors (IfADo), Dortmund, Germany.
authors.forename: Carsten
authors.initials: C
authors.lastname: Watzl
authors.affiliation: Immunology Department, Leibniz Research Center for Working Environment and Human Factors (IfADo), Dortmund, Germany.
authors.forename: Maren
authors.initials: M
authors.lastname: Claus
authors.affiliation: Medical Oncology Department, National Cancer Institute (NCI), Cairo, Egypt.
authors.forename: Ola
authors.initials: O
authors.lastname: Khorshid
authors.affiliation: Pharmacology and Toxicology Department, German University in Cairo (GUC), New Cairo, Egypt.
authors.forename: Laila
authors.initials: L
authors.lastname: Mahran
authors.affiliation: Microbiology and Immunology Department, German University in Cairo (GUC), New Cairo, Egypt.
authors.forename: Khaled
authors.initials: K
authors.lastname: Abou-Aisha
mesh_terms: D001483:Base Sequence; D001943:Breast Neoplasms / Q000097:blood / Q000235:genetics / Q000276:immunology / Q000473:pathology; D002469:Cell Separation; D002478:Cells, Cultured; D016207:Cytokines / Q000378:metabolism; D015536:Down-Regulation / Q000235:genetics; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D055785:Gene Knockdown Techniques; D006801:Humans; D007694:Killer Cells, Natural / Q000378:metabolism*; D035683:MicroRNAs / Q000737:chemistry / Q000235:genetics* / Q000378:metabolism; D055636:Receptors, Natural Cytotoxicity Triggering / Q000235:genetics* / Q000378:metabolism; D018709:Statistics, Nonparametric
chemical_list: D016207:Cytokines; C542542:MIRN146 microRNA, human; C540193:MIrn181 microRNA, human; D035683:MicroRNAs; D055636:Receptors, Natural Cytotoxicity Triggering