{"title":"Effects of hsa-piR-32877 Suppression with Antisense LNA GapmeRs on the Proliferation and Apoptosis of Human Acute Myeloid Leukemia Cells.","authors":"Sepideh Nasseri, Mohammadreza Sharifi, Valiollah Mehrzad","doi":"10.22088/IJMCM.BUMS.12.1.18","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":14152,"journal":{"name":"International Journal of Molecular and Cellular Medicine","volume":null,"pages":null},"PeriodicalIF":1.5000,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10629728/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"International Journal of Molecular and Cellular Medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.22088/IJMCM.BUMS.12.1.18","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
引用次数: 0
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.
期刊介绍:
The International Journal of Molecular and Cellular Medicine (IJMCM) is a peer-reviewed, quarterly publication of Cellular and Molecular Biology Research Center (CMBRC), Babol University of Medical Sciences, Babol, Iran. The journal covers all cellular & molecular biology and medicine disciplines such as the genetic basis of disease, biomarker discovery in diagnosis and treatment, genomics and proteomics, bioinformatics, computer applications in human biology, stem cells and tissue engineering, medical biotechnology, nanomedicine, cellular processes related to growth, death and survival, clinical biochemistry, molecular & cellular immunology, molecular and cellular aspects of infectious disease and cancer research. IJMCM is a free access journal. All open access articles published in IJMCM are distributed under the terms of the Creative Commons Attribution CC BY. The journal doesn''t have any submission and article processing charges (APCs).