Long non-coding RNA TUG1 inhibits apoptosis and inflammatory response in LPS-treated H9c2 cells by down-regulation of miR-29b

2018 ◽  
Vol 101 ◽  
pp. 663-669 ◽  
Author(s):  
Haifang Zhang ◽  
Hui Li ◽  
Ang Ge ◽  
Enyu Guo ◽  
Shuxia Liu ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
H9c2 Cells ◽  
Down Regulation ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals Long non-coding RNA ZFAS1 alleviates sepsis-induced myocardial injury via target miR-34b-5p/SIRT1

2021 ◽  
pp. 175342592110342
Author(s):  
Dan-Dan Chen ◽  
Hong-Wu Wang ◽  
Xing-Jun Cai
Keyword(s):  
Inflammatory Response ◽  
Cell Apoptosis ◽  
Myocardial Injury ◽  
Luciferase Assay ◽  
H9c2 Cell ◽  
Mrna Levels ◽  
H9c2 Cells ◽  
Western Blots ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Long non-coding RNA ZFAS1 is down-regulated in sepsis. However, whether ZFAS1 participates in sepsis-induced cardiomyopathy (SIC) remains largely unknown. LPS injection to rats was used to establish an in vivo sepsis model, while LPS stimulation with H9C2 cell was used to mimic an in vitro sepsis-induced myocardial injury model. Western blots and quantitative RT-PCR were performed to evaluate protein and mRNA levels, respectively. ELISA was conducted to determine cytokine levels in supernatant. Flow cytometry was used to test apoptosis. Dual-luciferase assay was performed to validate binding between ZFAS1 and miR-34b-5p, miR-34b-5p and SIRT1. Our data revealed that ZFAS1 and SIRT1 were down-regulated, while miR-34b-5p was up-regulated in LPS-induced H9C2 cells. Inhibition of miR-34b-5p or overexpression of ZFAS1 alleviated inflammatory response and cell apoptosis in LPS-stimulated H9C2 cells. A mechanism study revealed that ZFAS1 sponged miR-34b-5p and thus elevated expression of SIRT1, which was prohibited by miR-34b-5p. ZFAS1 alleviated inflammatory response and cell apoptosis in LPS-stimulated H9C2 cells via the miR-34b-5p/SIRT1 axis, providing novel potential therapeutic targets for SIC.

scholarly journals Knockdown of long non-coding RNA NEAT1 relieves the inflammatory response of spinal cord injury through targeting miR-211-5p/MAPK1 axis

Bioengineered ◽  
2021 ◽  
Vol 12 (1) ◽  
pp. 2702-2712
Author(s):  
Qing An ◽  
Zipeng Zhou ◽  
Yi Xie ◽  
Yu Sun ◽  
Haixiang Zhang ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Inflammatory Response ◽  
Non Coding Rna ◽  
Cord Injury ◽  
Long Non Coding Rna

scholarly journals The silencing of long non-coding RNA ANRIL suppresses invasion, and promotes apoptosis of retinoblastoma cells through the ATM-E2F1 signaling pathway

2018 ◽  
Vol 38 (6) ◽  
Author(s):  
Yang Yang ◽  
Xiao-Wei Peng
Keyword(s):  
Protein Expression ◽  
Signaling Pathway ◽  
Inhibitory Effect ◽  
Down Regulation ◽  
Reading Frame ◽  
Non Coding Rna ◽  
Retinoblastoma Cells ◽  
Human Retinoblastoma ◽  
Y79 Cells ◽  
Long Non Coding Rna

As one of the most common primary intraocular carcinomas, retinoblastoma generally stems from the inactivation of the retinoblastoma RB1 gene in retinal cells. Antisense non-coding RNA in the INK4 locus (ANRIL), a long non-coding RNA (lncRNA), has been reported to affect tumorigenesis and progression of various cancers, including gastric cancer and non-small cell lung cancer. However, limited investigations emphasized the role of ANRIL in human retinoblastoma. Hence, the current study was intended to investigate the effects of ANRIL on the proliferation, apoptosis, and invasion of retinoblastoma HXO-RB44 and Y79 cells. The lentivirus-based packaging system was designed to aid the up-regulation of ANRIL and ATM expressions or employed for the down-regulation of ANRIL in human retinoblastoma cells. Afterward, ANRIL expression, mRNA and protein expression of ATM and E2F1, and protein expression of INK4b, INK4a, alternate reading frame (ARF), p53 and retinoblastoma protein (pRB) were determined in order to elucidate the regulation effect associated with ANRIL on the ATM-E2F1 signaling pathway. In addition, cell viability, apoptosis, and invasion were detected accordingly. The results indicated that the down-regulation of ANRIL or up-regulation of ATM led to an increase in the expressions of ATM, E2F1, INK4b, INK4a, ARF, p53, and pRB. The silencing of ANRIL or up-regulation of ATM exerted an inhibitory effect on the proliferation and invasion while improving the apoptosis of HXO-RB44 and Y79 cells. In conclusion, the key observations of our study demonstrated that ANRIL depletion could act to suppress retinoblastoma progression by activating the ATM-E2F1 signaling pathway. These results provide a potentially promising basis for the targetted intervention treatment of human retinoblastoma.

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

Down-regulation of long non-coding RNA GAS5-AS1 and its prognostic and diagnostic significance in hepatocellular carcinoma

2018 ◽  
Vol 22 (2) ◽  
pp. 227-236 ◽  
Author(s):  
Yingchao Wang ◽  
Wei Jing ◽  
Weijie Ma ◽  
Chunzi Liang ◽  
Hongyan Chai ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Down Regulation ◽  
Diagnostic Significance ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals Long Non-Coding RNA H19 Protects H9c2 Cells against Hypoxia-Induced Injury by Targeting MicroRNA-139

2017 ◽  
Vol 44 (3) ◽  
pp. 857-869 ◽  
Author(s):  
Li-Cheng Gong ◽  
Hai-Ming Xu ◽  
Gong-Liang Guo ◽  
Tao Zhang ◽  
Jing-Wei Shi ◽  
...  
Keyword(s):  
Cell Viability ◽  
Cell Injury ◽  
Myocardial Cell ◽  
Mtor Pathway ◽  
Migration And Invasion ◽  
H9c2 Cells ◽  
Hypoxic Injury ◽  
Downstream Target ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Background/Aims: Acute myocardial infarction (AMI) occurs when blood supply to the heart is diminished (ischemia) for long time; ischemia is primarily caused due to hypoxia. The present study evaluated the effects of long non-coding RNA H19 on hypoxic rat H9c2 cells and mouse HL-1 cells. Methods: Hypoxic injury was confirmed by measuring cell viability, migration and invasion, and apoptosis using MTT, Transwell and flow cytometry assays, respectively. H19 expression after hypoxia was estimated by qRT-PCR. We then measured the effects of non-physiologically expressed H19, knockdown of miR-139 with or without H19 silence, and abnormally expressed Sox8 on hypoxia-induced H9c2 cells. Moreover, the interacted miRNA for H19 and downstream target gene were virtually screened and verified. The involved signaling pathways and the effects of abnormally expressed H19 on contractility of HL-1 cells were explored via Western blot analysis. Results: Hypoxia induced decreases of cell viability, migration and invasion, increase of cell apoptosis and up-regulation of H19. Knockdown of H19 increased hypoxia-induced injury in H9c2 cells. H19 acted as a sponge for miR-139 and H19 knockdown aggravated hypoxia-induced injury by up-regulating miR-139. Sox8 was identified as a target of miR-139, and its expression was negatively regulated by miR-139. The mechanistic studies revealed that overexpression of Sox8 might decrease hypoxia-induced cell injury by activating the PI3K/AKT/mTOR pathway and MAPK. Besides, H19 promoted contractility of HL-1 cells. Conclusion: These findings suggest that H19 alleviates hypoxia-induced myocardial cell injury by miR-139-mediated up-regulation of Sox8, along with activation of the PI3K/AKT/mTOR pathway and MAPK.

scholarly journals The Long Non-Coding RNA CRNDE Promotes Colorectal Carcinoma Progression by Competitively Binding miR-217 with TCF7L2 and Enhancing the Wnt/β-Catenin Signaling Pathway

2017 ◽  
Vol 41 (6) ◽  
pp. 2489-2502 ◽  
Author(s):  
Bo Yu ◽  
Xuan Ye ◽  
Qiong Du ◽  
Bin Zhu ◽  
Qing Zhai
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Signaling Pathway ◽  
Western Blotting ◽  
Migration And Invasion ◽  
Down Regulation ◽  
Over Expression ◽  
Non Coding Rna ◽  
Colorectal Cancer Cells ◽  
Long Non Coding Rna

Background/Aims: The long non-coding RNA colorectal neoplasia differentially expressed (CRNDE) contributes to the proliferation and migration of tumors. However, its molecular mechanism underlying gastric cancer remains unknown. In the present study, we investigated whether CRNDE was involved in the development of colorectal cancer via the binding of microRNA (miR)-217 with transcription factor 7-like 2 (TCF7L2) to enhance the Wnt signaling pathway. Methods: Quantitative polymerase chain reaction was used to detect CRNDE, miR-217 and TCF7L2 in colorectal cancer tissues and cells. The CCK-8 assay, wound healing assay, and Transwell assay were used to detect cell proliferation, migration and invasion, respectively. Western blotting and luciferase activity assays were used to identify CRNDE and TCF7L2 as one of the direct targets of miR-217. The activity of the Wnt/β-catenin signaling pathway was analyzed by the TOPflash assay, and the subcellular localization of β-catenin and TCF7L2 was analyzed by western blotting and confocal microscopy. Results: In this study, we found that high expression of CRNDE is negatively correlated with low expression of miR-217 in colorectal cancer tissue and colorectal cancer cells. The dual luciferase reporter analysis showed that miR-217 is bound to CRNDE and TCF7L2 and negatively regulate their expression. CRNDE down-regulation inhibited the cell proliferation, migration and invasion in vitro and in vivo and the inhibitions were both completely blocked after miR-217 inhibition or TCF7L2 overexpression. Finally, TOPflash analysis showed that the activity of Wnt/β-catenin signaling is inhibited by CRNDE down-regulation and rescued by TCF7L2 over-expression. Consistently immunostaining and western blotting analysis showed that the expression of b-catenin and TCF7L2 in the nucleus was significantly decreased by CRNDE down-regulation and was rescued by TCF7L2 over-expression. Conclusions: The present study suggest that CRNDE involves in the cell proliferation, migration and invasion of colorectal cancer cells via increasing the expression of TCF7L2 and activity of Wnt/β-catenin signaling through binding miR-217 competitively.

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