scholarly journals Long non‑coding RNA HOXA‑AS2 promotes the expression levels of hypoxia‑inducible factor‑1α and programmed death‑ligand 1, and regulates nasopharyngeal carcinoma progression via miR‑519

2020 ◽  
Vol 20 (5) ◽  
pp. 1-1
Author(s):  
Shuyong Wang ◽  
Huizeng You ◽  
Sa Yu
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Hypoxia Inducible Factor ◽  
Expression Levels ◽  
Hypoxia Inducible Factor 1 ◽  
Non Coding Rna ◽  
Programmed Death ◽  
Long Non Coding Rna

scholarly journals The HIF-1α antisense long non-coding RNA drives a positive feedback loop of HIF-1α mediated transactivation and glycolysis

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Fang Zheng ◽  
Jianing Chen ◽  
Xiaoqian Zhang ◽  
Zifeng Wang ◽  
Jiewen Chen ◽  
...  
Keyword(s):  
Hypoxia Inducible Factor ◽  
Hypoxia Inducible Factor 1 ◽  
Non Coding Rna ◽  
Cancer Phenotype ◽  
Nuclear Ribonucleoprotein ◽  
Heterogeneous Nuclear Ribonucleoprotein F ◽  
Long Non Coding Rna ◽  
Aggressive Breast Cancer

AbstractHypoxia-inducible factor-1 (HIF-1) is a master driver of glucose metabolism in cancer cells. Here, we demonstrate that a HIF-1α anti-sense lncRNA, HIFAL, is essential for maintaining and enhancing HIF-1α-mediated transactivation and glycolysis. Mechanistically, HIFAL recruits prolyl hydroxylase 3 (PHD3) to pyruvate kinase 2 (PKM2) to induce its prolyl hydroxylation and introduces the PKM2/PHD3 complex into the nucleus via binding with heterogeneous nuclear ribonucleoprotein F (hnRNPF) to enhance HIF-1α transactivation. Reciprocally, HIF-1α induces HIFAL transcription, which forms a positive feed-forward loop to maintain the transactivation activity of HIF-1α. Clinically, high HIFAL expression is associated with aggressive breast cancer phenotype and poor patient outcome. Furthermore, HIFAL overexpression promotes tumor growth in vivo, while targeting both HIFAL and HIF-1α significantly reduces their effect on cancer growth. Overall, our results indicate a critical regulatory role of HIFAL in HIF-1α-driven transactivation and glycolysis, identifying HIFAL as a therapeutic target for cancer treatment.

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.

scholarly journals Long non‐coding RNA ROR promotes proliferation, migration and chemoresistance of nasopharyngeal carcinoma

2016 ◽  
Vol 107 (9) ◽  
pp. 1215-1222 ◽  
Author(s):  
Li Li ◽  
Miao Gu ◽  
Bo You ◽  
Si Shi ◽  
Ying Shan ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Nano-Coated si-SNHG14 Regulated PD-L1 Expression and Decreased Epithelial-Mesenchymal Transition in Nasopharyngeal Carcinoma Cells

2021 ◽  
Vol 17 (10) ◽  
pp. 1993-2002
Author(s):  
Haoran Yu ◽  
Chen Zhang ◽  
Wanpeng Li ◽  
Xicai Sun ◽  
Quan Liu ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Animal Experiments ◽  
Loss Of Function ◽  
Mesenchymal Transition ◽  
Non Coding Rna ◽  
Long Non Coding Rna ◽  
Tumor Agent

To investigate the expression characteristics of long non-coding RNA SNHG14 in nasopharyngeal carcinoma (NPC) and its effects on epithelial-mesenchymal transition and development of nano-coated si-SNHG14 as an anti-tumor agent. The SNHG14 expression in cancerous and adjacent non-cancerous tissues was monitored using reverse transcriptionpolymerase chain reaction (RT-PCR). Gain- and loss-of-function experiments tested the regulation of SNHG14, miR- 5590-3p, and ZEB1 on PD-L1. The binding association between the above three factors was verified using bioinformatics analysis. EMT-related E-cadherin, N-cadherin, and Vimentin were tested using Western blot. Animal experiments in nude mice verified the function of SNHG14 in the EMT of NPC in vivo. The nano-coated si-SNHG14 was developed as an anti-tumor agent and was verified NPC cell in vitro. SNHG14 was upregulated in NPC tissues. Knocking down SNHG14 markedly inhibited the EMT of NPC. Additionally, the expression of ZEB1 was positively related to that of the SNHG14, while it was inversely correlated with that of miR-5590-3p. Moreover, ZEB1 transcription upregulated PD-L1 and promoted the EMT, while SNHG14 could accelerate the EMT of NPC in vivo by regulating the PD-1 and PD-L1. SNHG14-miR-5590- 3p-ZEB1 positively regulated PD-L1 and facilitate the EMT of NPC. Nano-coated si-SNHG14 significantly downregulated PD-L1 expression and decreased EMT.

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.

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