Effects of hsa-piR-32877 Suppression with Antisense LNA GapmeRs on the Proliferation and Apoptosis of Human Acute Myeloid Leukemia Cells

(2023) Effects of hsa-piR-32877 Suppression with Antisense LNA GapmeRs on the Proliferation and Apoptosis of Human Acute Myeloid Leukemia Cells. International Journal of Molecular and Cellular Medicine. pp. 18-29. ISSN 2251-9637

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Abstract

Acute myeloid leukemia (AML) is an invasive form of hematologic malignancies which results in the overproduction of myeloid cells in the bone marrow. Aberrant expression of piwi- interacting RNAs (piRNAs) which belong to small non-coding RNAs, play important roles in different cancer cells' progress. hsa- piR- 32877 is up-regulated in AML. Down regulation of hsa-piR-32877 by antisense LNA GapmeRs could be potential for suppression of myeloid cell proliferation and induce myeloid cell apoptosis. We have blocked the expression of hsa-piR-32877 by antisense LNA GapmeRs in human bone marrow blast cells, and the M-07e cell line. Samples were transfected with antisense LNA GapmeRs at 24, 48, and 72 hours. The Quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) was performed to investigate the expression of hsa-piR-32877, CASP3, and CASP9. Both CASP3 and CASP9 play important roles in apoptosis. Cell proliferation was studied via CFSE (carboxyfluorescein diacetate succinimidyl ester) assay. Results showed that hsa-piR-32877 was down-regulated by antisense LNA GapmeRs in the patient and cell line samples. Also, after transfection, cell proliferation and apoptosis decreased and increased, respectively. Our data suggested that hsa-piR-32877 suppression may act as a novel therapeutic method for the inhibition of human leukemic cells proliferation in AML.

Item Type: Article
Keywords: Acute myeloid leukemia Antisense LNA GapmeRs hsa-piR-32877 CASP3 CASP9 piwi-interacting rna expression DNA methylation biogenesis Research & Experimental Medicine
Page Range: pp. 18-29
Journal or Publication Title: International Journal of Molecular and Cellular Medicine
Journal Index: ISI
Volume: 12
Number: 1
Identification Number: https://doi.org/10.22088/ijmcm.Bums.12.1.18
ISSN: 2251-9637
Depositing User: خانم ناهید ضیائی
URI: http://eprints.mui.ac.ir/id/eprint/27095

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