scholarly journals Long noncoding RNA UBE2R2-AS1 promotes glioma cell apoptosis via targeting the miR-877-3p/TLR4 axis

2019 ◽  
Vol Volume 12 ◽  
pp. 3467-3480 ◽  
Author(s):  
Wu Xu ◽  
Guo-Qing Hu ◽  
Clive Da Costa ◽  
Jun-Hai Tang ◽  
Qing-Rui Li ◽  
...  
Keyword(s):  
Cell Apoptosis ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Glioma Cell

scholarly journals Long noncoding RNA-MEG3 contributes to myocardial ischemia–reperfusion injury through suppression of miR-7-5p expression

2019 ◽  
Vol 39 (8) ◽  
Author(s):  
Liyuan Zou ◽  
Xiaokun Ma ◽  
Shuo Lin ◽  
Bingyuan Wu ◽  
Yang Chen ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Caspase 3 ◽  
Ischemia Reperfusion Injury ◽  
Cell Model ◽  
Ischemia Reperfusion ◽  
Luciferase Reporter

Abstract Long noncoding RNA (lncRNA) maternally expressed gene 3 (MEG3) plays an important role in protection of ischemia–reperfusion (I/R) injury in brain and liver. However, role of MEG3 in myocardial I/R injury remains unclear. Here, the role of MEG3 in protection of myocardial I/R injury and its association with microRNA-7-5p (miR-7-5p) was investigated using rat cardiac I/R model and myocardial I/R cell model. Our results showed that MEG3 was significantly up-regulated and miR-7-5p was significantly down-regulated after I/R. Following I/R, the levels of intact PARP and intact caspase-3 were reduced, while the cleaved fragments of PARP and caspase-3 were increased. TUNEL assay showed an increase in cardiomyocyte apoptosis after I/R. The levels of I/R-induced creatine kinase (CK) and lactate dehydrogenase (LDH) were inhibited by knockdown of MEG3 (siMEG3). SiMEG3 increased cell proliferation and inhibited cell apoptosis after I/R. In contrast, overexpression of MEG3 increased the I/R-induced CK and LDH activities and cell apoptosis and decreased cell proliferation. The dual-luciferase reporter system showed a direct binding of MEG3 to miR-7-5p. The level of miR-7-5p was negatively associated with the change in levels of MEG3 in H9c2 cells. The levels of intact RARP1 and caspase-3 were significantly increased by knockdown of MEG3. Co-transfection of miR-7-5p inhibitor with siMEG3 activates CK and LDH, significantly decreased cell proliferation, increased cell apoptosis, and decreased intact poly(ADP-ribose) polymerase 1 (PARP1) and caspase-3. In summary, down-regulation of MEG3 protects myocardial cells against I/R-induced apoptosis through miR-7-5p/PARP1 pathway, which might provide a new therapeutic target for treatment of myocardial I/R injury.

scholarly journals Long Noncoding RNA KCNQ1OT1 Accelerates the Progression of Ovarian Cancer via MicroRNA-212-3/LCN2 Axis

2020 ◽  
Vol 28 (2) ◽  
pp. 135-146 ◽  
Author(s):  
Xiaoqin Lu ◽  
Fuying Wang ◽  
Meizhou Fu ◽  
Yuankun Li ◽  
Lijun Wang
Keyword(s):  
Ovarian Cancer ◽  
Cell Growth ◽  
Cell Apoptosis ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Migration And Invasion ◽  
Skov3 Cells ◽  
Direct Target ◽  
Rna Interaction ◽  
Cancer Tissues

Long noncoding RNA KCNQ1OT1 (KCNQ1OT1) has been identified to be deregulated in several kinds of cancers. However, its expression pattern and functions in ovarian cancer remain unknown. Bioinformatics analysis showed that miR-212-3p, an identified suppressor in ovarian cancer, was a direct target of KCNQ1OT1, suggesting that KCNQ1OT1 may play a role in ovarian cancer progression via targeting miR-212-3p. Here we aimed to explore the effect of KCNQ1OT1 on the carcinogenesis of ovarian cancer, as well as to investigate miR-212-3p roles in this process. The expression of KCNQ1OT1 and miR-212-3p in ovarian cancer tissues and cells was detected by qPCR. MTT, flow cytometry, wound healing, Transwell chambers, and in vivo tumor formation assays were carried out to assess cell proliferation, apoptosis, migration, invasion, and tumorigenesis, respectively. RNA pulldown and luciferase gene reporter assays were used to evaluate the RNA‐RNA interaction. The results showed that KCNQ1OT1 was overexpressed in ovarian cancer tissues and cells, which closely associated with the advanced clinic process and poor prognosis in ovarian cancer patients. Upregulation of KCNQ1OT1 significantly enhanced cell growth, migration, and invasion and inhibited cell apoptosis via miR-212-3p. In addition, we identified that lipocalin2 (LCN2) was a direct target of miR-212-3p and functioned as an oncogene to promote cell growth and to inhibit cell apoptosis. Furthermore, we observed that KCNQ1OT1 overexpression significantly enhanced the tumorigenesis of SKOV3 cells, whereas this effect was significantly impaired when LCN2 expression was downregulated. Overall, the present study reveals that KCNQ1OT1 functions as an oncogene in ovarian cancer via targeting miR-212-3p/LCN2 axis, which might provide new markers and targets for ovarian cancer diagnosis and treatment.

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