z-logo
open-access-imgOpen Access
Inhibition of microRNA miR-92a induces apoptosis and necrosis in human acute promyelocytic leukemia
Author(s) -
Mohammadreza Sharifi,
Roya Salehi,
Yousof Gheisari,
Mohammad Kazemi
Publication year - 2014
Publication title -
advanced biomedical research
Language(s) - English
Resource type - Journals
ISSN - 2277-9175
DOI - 10.4103/2277-9175.125826
Subject(s) - acute promyelocytic leukemia , propidium iodide , microrna , apoptosis , antagomir , cancer research , leukemia , myeloid leukemia , annexin , k562 cells , transfection , medicine , microbiology and biotechnology , biology , cell culture , programmed cell death , immunology , retinoic acid , gene , biochemistry , genetics
Background: MicroRNAs (miRNAs) are endogenous non-coding RNAs, 19-25 nucleotides in length, involved in post-transcriptional regulation of gene expression in a considerable majority of mRNAs. Different aspects of cellular activities like cell growth, proliferation, and differentiation are regulated by miRNAs through their regulatory effects on particular RNA species. In many tumors, up- or down-regulation of different miRNAs has been reported. In acute myeloid leukemia, up-regulation of miR-92a has been reported in human in-vitro studies. Materials and Methods: We performed inhibition of miR-92a in an acute promyelocytic leukemia cell line (HL-60), using locked nucleic acid (LNA) Antagomir. At different time points after LNA-anti-miR92a transfection, qRT-Real-Time-polymerase chain reaction (PCR) and Annexin-V/Propidium Iodide staining were performed and the data was analyzed using the Kruskal-Wallis and Mann-Whitney tests. Results: The assessment of the apoptosis and necrosis indicates that miR-92a inhibition can decrease the viable HL-60 cells and this is at least partially due to induction of apoptosis. Conclusion: These findings suggest the inhibition of miR-92a as a novel approach for treatment of Acute Promyelocytic Leukemia (APL)

The content you want is available to Zendy users.

Already have an account? Click here to sign in.
Having issues? You can contact us here