scholarly journals Overexpressed long noncoding RNA TUG1 affects the cell cycle, proliferation, and apoptosis of pancreatic cancer partly through suppressing RND3 and MT2A

2019 ◽  
Vol Volume 12 ◽  
pp. 1043-1057 ◽  
Author(s):  
Bingqing Hui ◽  
Yetao Xu ◽  
Benpeng Zhao ◽  
Hao Ji ◽  
Zhonghua Ma ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Pancreatic Cancer ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Proliferation And Apoptosis

scholarly journals Long Noncoding RNA NORAD/MiR-26a-5p/NAMPT (Visfatin) Axis Regulates Proliferation and Apoptosis of Human Osteosarcoma Cells

2020 ◽  
Author(s):  
Gong Cheng ◽  
Botao Huang ◽  
Zhilin Cao ◽  
Tongqing Zhang ◽  
Yuchi Zhao ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Luciferase Reporter ◽  
Apoptosis Resistance ◽  
Tissue Samples ◽  
Protein Levels ◽  
Human Osteosarcoma Cells ◽  
Proliferation And Apoptosis ◽  
U2os Cells

Abstract Background: Visfatin is a novel adipokine, also known as a nicotinamide phosphorybosyltransferase (NAMPT) that is reported to promote the progression of osteosarcoma. The research sought to determine the regulatory network underlying NAMPT on osteosarcoma (OS).Method: The OS tissues and paired normal controls were collected from 45 OS patients. The binding relationship between microRNA-26a-5p (miR-26a-5p) and two genes (NAMPT and NORAD) were predicted by TargetScan V7.2 and confirmed by dual-luciferase reporter assay. To reveal the function of long noncoding RNA NORAD/miR-26a-5p/NAMPT axis on cell viability, cell cycle and apoptosis of U2OS cells, CCK-8 and flow cytometry assays, examination of apoptosis-associated molecules (Bcl-2, Bax, cleaved (C)-caspase-3) were performed. The mRNA and protein levels were separately examined by RT-qPCR and Western blot. Results: NAMPT and NORAD expressions were increased in OS tissue samples, while miR-26a-5p expression was decreased. Functionally, NORAD functions as a ceRNA of miR-136-5p to competitively target NAMPT. Furthermore, miR-26a-5p overexpression inhibited viability, cell cycle and apoptosis resistance of U2OS cells by down-regulating NAMPT along with change the expressions of apoptosis-related molecules. NORAD overexpression promoted viability, cell cycle and apoptosis resistance of U2OS cells by down-regulating MiR-26a-5p along with changes of the expressions of apoptosis-related molecules.Conclusion: LncRNA NORAD, serving as a ceRNA of miR-26a-5p, promoted proliferation and apoptosis resistance of U2OS cells by upregulation of NAMPT.

scholarly journals Long noncoding RNA KCNQ1OT1 targets miRNA let-7a-5p to regulate Osteoarthritis development and progression

2021 ◽  
Author(s):  
hafiza sobia ramzan ◽  
Kashif Aziz Ahmad
Keyword(s):  
Cell Viability ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Molecular Mechanisms ◽  
Luciferase Assay ◽  
Common Disease ◽  
Functional Roles ◽  
Non Coding Rna ◽  
Proliferation And Apoptosis ◽  
Long Non Coding Rna

Background: Osteoarthritis (OA) is a common disease of the joints among old populace until today. The treatment possibilities and roles of miRNA and long non-coding RNA (lncRNA) in therapy of OA has previously been explored. However, the functional roles of Long noncoding RNA KCNQ1OT1 and miRNA let-7a-5p on Osteoarthritis development and progression remains unclear. This study aimed at investigating the influence of KCNQ1OT1 on let-7a-5p in moderation of OA development and advancement. Materials and Methods: RT-qPCR examined expression of KCNQ1OT1and let-7a-5p in cultured human primary chondrocyte cell lines. Cell transfection overexpressed or knocked down the genes and CCK-8 assay measured cell viability in the proliferation biomarkers Ki87 and PCNA. While caspase-8 and caspase-3 activity determined rate of apoptosis. Furthermore, luciferase assay analyzed the luciferase activity and western blotting analysis determined the protein expression of KCNQ1OT1 and let-7a-5p in proliferation and apoptosis biomarkers. Results: The results demonstrated that KCNQ1OT1 is upregulated in OA-mimic cells and promotes the cell viability. KCNQ1OT1 knockdown suppresses cell viability of OA cells. Furthermore KCNQ1OT1 directly binds the 3'-UTR of let-7a-5p to negatively regulate let-7a-5p expression and OA progression. While upregulated let-7a-5p abolishes the proliferation effect of KCNQ1OT1 in OA cells. Conclusion: In summary, our study provides further insights into the underlying molecular mechanisms of KCNQ1OT1 and let-7a-5p suggesting a novel therapeutic approach to OA

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