scholarly journals Long non‐coding RNA growth arrest‐specific 5 and its targets, microRNA‐21 and microRNA‐140, are potential biomarkers of allergic rhinitis

2021 ◽  
Author(s):  
Ji Song ◽  
Taojiao Wang ◽  
Yandan Chen ◽  
Ruixiang Cen
Keyword(s):  
Allergic Rhinitis ◽  
Growth Arrest ◽  
Non Coding Rna ◽  
Long Non Coding Rna ◽  
Potential Biomarkers

scholarly journals Long Non-coding RNA GAS5 Worsens Coronary Atherosclerosis Through MicroRNA-194-3p/TXNIP Axis

2021 ◽  
Author(s):  
Yanbing Li ◽  
Yu Geng ◽  
Boda Zhou ◽  
Xuejiao Wu ◽  
Ou Zhang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Coronary Atherosclerosis ◽  
Growth Arrest ◽  
Interacting Protein ◽  
Expression Levels ◽  
Thioredoxin Interacting Protein ◽  
Non Coding Rna ◽  
Proliferation And Apoptosis ◽  
Regulatory Effects ◽  
Long Non Coding Rna

AbstractIt is formerly conducted that long non-coding RNA growth arrest-specific 5 (GAS5) is involved in the process of coronary atherosclerosis (AS). The regulatory effects of GAS5 on the microRNA (miR)-194-3p/thioredoxin-interacting protein (TXNIP) axis in AS have been insufficiently explored yet. Thereafter, this work is started from GAS5/miR-194-3p/TXNIP axis in AS. AS rats were modeled to obtain their coronary vascular tissues and endothelial cells (ECs), in which GAS5, miR-194-3p, and TXNIP expression were tested. ECs were identified by immunohistochemistry. The mechanism among GAS5, miR-194-3p, and TXNIP was determined. ECs were transfected with inhibited GAS5 or overexpressed miR-194-3p to decipher their functions in proliferation and apoptosis of ECs in AS. Raised GAS5 and TXNIP and degraded miR-194-3p expression levels exhibited in AS. GAS5 bound to miR-194-3p while miR-194-3p targeted TXNIP. Depleting GAS5 or restoring miR-194-3p enhanced proliferation and depressed apoptosis of ECs in AS. This work clearly manifests that inhibited GAS5 facilitates the growth of ECs through miR-194-3p-targeted TXNIP in AS, consolidating the basal reference to the curing for AS.

Inducing cell growth arrest and apoptosis by silencing long non-coding RNA PCAT-1 in human bladder cancer

Tumor Biology ◽  
2015 ◽  
Vol 36 (10) ◽  
pp. 7685-7689 ◽  
Author(s):  
Li Liu ◽  
Yuchen Liu ◽  
Chengle Zhuang ◽  
Wen Xu ◽  
Xing Fu ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cell Growth ◽  
Growth Arrest ◽  
Human Bladder Cancer ◽  
Human Bladder ◽  
Cell Growth Arrest ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Down regulation of the long non-coding RNA PCAT-1 induced growth arrest and apoptosis of colorectal cancer cells

Life Sciences ◽  
2017 ◽  
Vol 188 ◽  
pp. 37-44 ◽  
Author(s):  
Lei Qiao ◽  
Xiangyu Liu ◽  
Yichao Tang ◽  
Zheng Zhao ◽  
Jilong Zhang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Growth Arrest ◽  
Down Regulation ◽  
Non Coding Rna ◽  
Colorectal Cancer Cells ◽  
Long Non Coding Rna

Effect of long non‐coding RNA growth arrest‐specific 5 on apoptosis in renal ischaemia/reperfusion injury

Nephrology ◽  
2019 ◽  
Vol 24 (4) ◽  
pp. 405-413 ◽  
Author(s):  
Xuemei Geng ◽  
Xialian Xu ◽  
Yi Fang ◽  
Shuan Zhao ◽  
Jiachang Hu ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Growth Arrest ◽  
Ischaemia Reperfusion Injury ◽  
Renal Ischaemia ◽  
Ischaemia Reperfusion ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Long non-coding RNA SNHG16, binding with miR-106b-5p, promoted cell apoptosis and inflammation in allergic rhinitis by up-regulating leukemia inhibitory factor to activate the JAK1/STAT3 signaling pathway

2021 ◽  
pp. 096032712110356
Author(s):  
Huajing Li ◽  
Fang Quan ◽  
Pengfei Zhang ◽  
Yuan Shao
Keyword(s):  
Allergic Rhinitis ◽  
Cell Apoptosis ◽  
Leukemia Inhibitory Factor ◽  
Cell Model ◽  
Inhibitory Factor ◽  
Luciferase Reporter ◽  
Stat3 Pathway ◽  
Non Coding Rna ◽  
Apoptosis And Inflammation ◽  
Long Non Coding Rna

Allergic rhinitis (AR) is a type I hypersensitive disease. Long non-coding RNA (lncRNA) SNHG16 acts as an oncogene in a variety of tumors and promotes the occurrence of inflammation in many inflammatory diseases. The study aims to investigate the expression of SNHG16 and its potential biological functions in AR. RT-qPCR results showed that the expression of SNHG16 in AR was up-regulated. The AR cell model was constructed by stimulating primary nasal mucosal epithelial cells from AR patients with IL-13. After knocking down the expression of lncRNA SNHG16, cell apoptosis was detected by flow cytometry, and the expression of inflammatory factors was detected by ELISA. The results showed that SNHG16 promoted cell apoptosis and inflammation. Then, bioinformatics analysis was used to screen miRNAs bound with SNHG16. Luciferase reporter gene assay and RNA pull-down experiment were used to verify the relationship. We found that the expression of miR-106b-5p was down-regulated and leukemia inhibitory factor (LIF) expression was up-regulated in the AR cell model. The expression of phospho-Janus kinase 1 and p-signal transducer and activator of transcription 3 (STAT3) were detected by Western blotting. Silencing the expression of LIF could inhibit the activity of JAK1/STAT3 pathway and further inhibit cell apoptosis and the occurrence of inflammation. Then transfected SNHG16 shRNA alone or together with miR-106b-5p antagomir into the AR cell model, we found that silencing the expression of SNHG16 down-regulated the expression of LIF and inhibited the activity of the JAK1/STAT3 pathway, cell apoptosis, and inflammation. However, miR-106b-5p antagomir weakened its inhibitory effects. The role of SNHG16 in AR was further verified by the ovalbumin-induced AR mouse model in vivo. In conclusion, SNHG16 up-regulates LIF expression by binding with miR-106b-5p, thus promoting the activity of JAK1/STAT3 pathway, and promoting the development of AR. These results provide new targets for the treatment of AR and may help reduce the damage caused by AR.

scholarly journals LncRNA GAS5 facilitates nasopharyngeal carcinoma progression through epigenetically silencing PTEN via EZH2

RSC Advances ◽  
2019 ◽  
Vol 9 (54) ◽  
pp. 31691-31698
Author(s):  
Dan Zhao ◽  
Yujie Li ◽  
Min Yu
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Growth Arrest ◽  
Cancer Development ◽  
Specific Transcript ◽  
Non Coding Rna ◽  
Long Non Coding Rna ◽  
Lncrna Gas5

Increasing evidence demonstrated that long non-coding RNA growth-arrest-specific transcript 5 (GAS5) serves as a critical regulator in cancer development and progression.

Sign in / Sign up

Export Citation Format

Share Document