MicroRNA-107 promotes apoptosis of acute myelocytic leukemia cells by targeting RAD51

Abstract

Introduction: This study aimed to investigate the role of microRNA (miRNA) that affects acute myelocytic leukemia (AML) and its potential molecular mechanism by constructing a miRNA-mRNA interaction network using bioinformatics methods. Material and methods: MicroRNA expression data of AML were retrieved from Gene Expression Omnibus (GEO) and analyzed by microarray analysis. Expression levels of miR-107 and RAD51 mRNA were detected by quantitative real time polymerase chain reaction (qRT-PCR). Protein expression of RAD51, pro-apoptotic protein Bax, apoptosis related protein CytC and anti-apoptotic protein Bcl-2 were determined by Western blot. The rate of cell apoptosis was detected by Annexin-V/PI. The predicted targeting relationship between miR-107 and the 3′UTR of RAD51 was first predicted by the online application TargetScan and then verified by dual-luciferase assay. Results: Acute myelocytic leukemia-associated genes (n = 197) and miRNAs (n = 1701) were retrieved from the database, the interaction network of miRNA-mRNA was constructed and the core position was occupied by RAD51. miR-107 exhibited a regulatory effect on RAD51 in which the mRNA and protein expression of RAD51 were both significantly inhibited by miR-107 mimics in vitro. Additionally, down-regulated expression of miR107 as well as up-regulated expression of RAD51 were detected not only in the plasma of AML patients compared to healthy volunteers, but also in AML cell lines compared to the normal bone marrow stromal cell line. Further study found that increased expression of miR-107 and the consequent down-regulation of RAD51 could aggravate the apoptosis of AML cells in vitro. Conclusions: Our present results showed that the crucial role of RAD51 and miR-107 in the apoptosis of AML cells, i.e., miR-107 promotes the apoptosis of AML cells through down-regulating the expression of RAD51.

Effects of miR-107 on Breast Cancer Cell Growth and Death via Regulation of the PTEN/AKT Signaling Pathway

“…Te number of invasive cells was lower in the miR-107 inhibitor group than in the blank and control miRNA groups, but there was no signifcant diference between the b groups. Furthermore, this shows that inhibiting miR-107 has a considerable inhibitory impact on it; confrming those fndings, researchers anticipate that by changing tumor cells into cells that support parenchymal cells in the completion of organ tasks, miR-107 will boost cell invasion and metastasis in breast cancer cell lines [19,20]. In addition, it is well known that in the biological behavior of cells, there is an indicator that can signifcantly monitor the degree of cell damage, namely apoptosis.…”

“…This suggests that miR-107 inhibition affects breast cancer cell growth and apoptosis. Breast cancer cells may be inhibited from autophagy, proliferation, and migration by HMGB1 [ 17 ]; in addition, several research studies have discovered that miR-107 controls PTX sensitivity via Wnt/-catenin signaling pathway, which targets TPD52 [ 18 – 20 ], [ 17 , 18 , 18 – 20 ]. The most dangerous and life-threatening behavior of cancer cells is invasion and metastasis.…”

Identification and Characterization of circRNAs in Non-Lactating Dairy Goat Mammary Glands Reveal Their Regulatory Role in Mammary Cell Involution and Remodeling

“…Among them, these apoptosis-related genes participate in the regulation of apoptosis, the JAK-STAT signaling pathway, the FoxO signaling pathway, the PI3K-Akt signaling pathway, the TNF signaling pathway, and other signaling pathways (Figure S19). It has been reported that miR-103a-3p and miR-107-3p are involved in the regulation of apoptosis [62,63]. Both chi-miR-103-3p and chi-miR-107-3p are in the ceRNA network related to apoptosis.…”

lncRNA GAPLINC regulates vascular endothelial cell apoptosis in atherosclerosis

“…Long non-coding RNAs (lncRNAs) are non-protein-coding RNAs that are longer than 200 nucleotides [6,7]. LncRNAs have been confirmed to play a key role in an increasing number of diseases [8][9][10]. Although many lncRNAs have been found to be involved in atherosclerosis, compared with coding molecules, a relatively small number of genes has been studied.…”